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Full text of "Reproductive hazards and military service : what are the risks of radiation, Agent Orange, and Gulf War exposures? : hearing before the Committee on Veterans' Affairs, United States Senate, One Hundred Third Congress, second session, August 5, 1994"

Uj S. Hrg. 103-983 

REPRODUCTIVE HAZARDS AND MILITARY 

SERVICE: WHAT ARE THE RISKS OF RADIATION, 

AGENT ORANGE, AND GULF WAR EXPOSURES? 

Y 4. V 64/4: S, HRG, 103-983 

Reproductive Hazards and Hilitary S. . . 

HEARING 

BEFORE THE 

COMMITTEE ON VETERANS' AFFAIRS 
UNITED STATES SENATE 

ONE HUNDRED THIRD CONGRESS 
SECOND SESSION 



AUGUST 5, 1994 



Printed for the use of the Committee on Veterans' Affairs 







""^>^,: 



S. Hrg. 103-983 

REPRODUCTIVE HAZARDS AND MILITARY 

SERVICE: WHAT ARE THE RISKS OF RADIATION, 

AGENT ORANGE, AND GULF WAR EXPOSURES? 



HEARING 

BEFORE THE 

COMMITTEE ON VETERANS' AFFAIRS 
UNITED STATES SENATE 

ONE HUNDRED THIRD CONGRESS 

SECOND SESSION 



AUGUST 5, 1994 



Printed for the use of the Committee on Veterans' Affairs 




U.S. GOVERNMENT PRINTING OFFICE 
WASHINGTON : 1995 



For sale by the U.S. Government Printing Office 
Superintendent of Documents, Congressional Sales Office, Washington, DC 20402 
ISBN 0-16-046908-2 



COMMITTEE ON VETERANS' AFFAIRS 
JOHN D. ROCKEFELLER IV, West Virginia, Chairman 

DENNIS DeCONCINI, Arizona FRANK H. MURKOWSKI, Alaska 

GEORGE J. MITCHELL, Maine STROM THURMOND, South Carolina 

BOB GRAHAM, Florida ALAN K. SIMPSON, Wyoming 

DANIEL K. AKAKA, Hawaii ARLEN SPECTER, Pennsylvania 

THOMAS A. DASCHLE, South Dakota JAMES M. JEFFORDS, Vermont 
BEN NIGHTHORSE CAMPBELL, Colorado 

Jim Gottlieb, Chief Counsel / Staff Director 
John H. Moseman, Minority Staff Director /Chief Counsel 

(II) 



CONTENTS 



AUGUST 5, 1994 

Page 
Reproductive Hazards and Military Service: What are the Risks of Radiation, 
Agent Orange, and Gulf War Exposures? 1 

STATEMENTS BY COMMITTEE MEMBERS 

Chairman John D. Rockefeller FV 1 

Prepared statement of Chairman Rockefeller 53 

Senator Thomas A. Daschle 54 

Senator Frank H. Murkowski 137 

WITNESSES 

Albuck, Kelli, wife of Persian Gulf War veteran, Barrington, IL 15 

Prepared statement of Mrs. Albuck 209 

Bailey, Sue, M.D., Deputy Assistant Secretary for Professional Affairs and Quality 

Assurance, Department of Defense 43 

Chan, Kwai-Cheung, Issue Area Director, Program Evaluation and Methodology 

Division, U.S. General Accounting Office 34 

Prepared statement of Mr. Chan 265 

Falk, Henry, M.D., Director, Environmental Hazards and Health Effects Division, 
Centers for Disease Control and Prevention, accompanied by Colleen Boyle, M.D., 

Section Chief, Birth Defects and Developmental Disabilities Division 43 

Prepared statement of Dr. Falk 274 

Farland, William, M.D., Director, Office of Health and Environmental Assessment, 

U.S. Environmental Protection Agency 42 

Goonan, Thomas M., Vietnam veteran. Associate Director, Agent Orange Family 

Assistance Program, Utah State University, Logan, UT 12 

Prepared statement of Mr. Goonan 205 

Mather, Susan, M.D., Assistant Chief Medical Director, Environmental Medicine 
and Public Health, Department of Veterans Affairs, accompanied by Frances M. 

Murphy, M.D., M.P.H., Acting Director, Environmental Agents Service 48 

Prepared statement of Dr. Mather 270 

Maxwell, Jacqueline C, widow of atomic veteran, director. Atomic Parents, 

National Association of Radiation Survivors, Menlo Park, CA 4 

Prepared statement of Mrs. Maxwell 139 

Miller, Stephen G., Persian Gulf War veteran, San Antonio, TX 18 

Prepared statement of Mr. Miller 210 

Parrish, Albert G. "Smoky," atomic veteran. Mayor, Hackensack, MN 9 

Prepared statement of Mr. Parrish 145 

Paul, Maureen E., M.D., M.P.H., director, Occupational and Environmental Repro- 
ductive Hazards Center, University of Massachusetts Medical Center, 

Worcester, MA 27 

Prepared statement of Dr. Paul 236 

Schwartz, Linda S., R.N., M.S.N. , doctoral student, Department of Epidemiology 

and Public Health, School of Medicine , Yale University, New Haven, CT 33 

Prepared statement of Ms. Schwartz 254 

(III) 



IV 

Siebert, George, Assistant Deputy Under Secretary for Safety and Occupational 
Health, Department of Defense 45 

Silbergeld, Ellen K., Ph.D., professor of epidemiology and toxicology. Department of 
Epidemiology and Preventative Medicine, University of Maryland School of 

Medicine, Baltimore, MD 30 

Prepared statement of Dr. Silbergeld 243 

Wellstone, Hon. Paul, a U.S. Senator from the State of Minnesota 2 

APPENDICES 

Appendix 1. — Prepared statements of Committee members 53 

Appendix 2. — Prepared statements of witnesses 139 

Appendix 3. — Statements submitted for the record 
Anonymous note regarding pregnancy warnings to U.S. troops in the Persian 

Gulf 305 

Ayers, Melanie 298 

Funmaker, Walter 285 

Gemmrig, James R 290 

Haines, Richard Henry 308 

Hibben, Lawrence 282 

Mayerhofer, Hilmar 288 

Smeltzer, David L 292 

Smith, David A 307 

Sullivan, Kim S 303 

Toranto, E. F. Gene 279 

Zumwalt, Jr., Elmo R., Admiral, USN (ret.) 323 

Appendix 4. — ^Written questions and the responses 
Chairman Rockefeller to: 

Centers for Disease Control and Prevention 381 

Department of Defense 389 

Environmental Protection Agency 407 

General Accounting Office 410 

Mather, Dr. Susan 418 

Paul, Dr. Maureen E 416 

Silbergeld, Dr. Ellen K. 413 

Appendix 5. — EPA dioxin reassessment and articles regarding reproductive 

hazards 425 

Appendix 6. — Research on toxic exposures 435 



REPRODUCTIVE HAZARDS AND MILITARY 
SERVICE: WHAT ARE THE RISKS OF 
RADIATION, AGENT ORANGE, AND GULF WAR 
EXPOSURES? 



FRroAY, AUGUST 5, 1994 

U.S. Senate 
Committee on Veterans' Affairs 

Washington, DC. 

The Committee met, pursuant to notice, at 10:35 a.m. in SH-216, 
Hart Senate Office Building, Hon. John D. Rockefeller IV (Chairman 
of the Committee) presiding. 

Present: Senators Rockefeller and Daschle. 

Also present: Senator Wellstone. 

Also present (staff): Jim GottUeb, chief counsel/staff" director; Diana 
M. Zuckerman, professional staff member; Patricia Olson, congressio- 
nal science fellow; and John Moseman, minority staff director/chief 
coimsel. 

OPENING STATEMENT OF CHAIRMAN ROCKEFELLER 

Chairman ROCKEFELLER. Good morning, everyone. This hearing 
will come to order. 

From the very earliest days of our Nation's history, our Govern- 
ment has expressed its commitment to help veterans who are 
wounded in battle. But unseen hazards which are unrelated to the 
battlefield can also create devastating medical problems, and we're 
beginning to understand that. Those imseen hazards may not become 
obvious until long after these men and women have left military 
service, but they are injuries nevertheless. 

As the nature of military service changes, we must rethink 
veterans' medical needs. Just consider the humanitarian military 
activities in Rwanda this week or the Persian Gulf War, where 
months of waiting in the desert and a few days of ground war may 
have created more medical problems from toxic exposures than from 
all of the battle wounds. Yet these veterans were truly injured, even 
if we do not yet understand those injuries. 

Today, when we try to meet the health needs of veterans, we need 
to continue to consider physical and mental battle wounds and the 
scars that they leave behind, but we also need to think about the 
more subtle and sometimes long-term risks of unseen enemies, such 
as diseases and chemical exposures. 



Today this Committee will focus on how these unseen enemies may 
eventually prevent veterans from having children or may increase the 
likelihood of birth defects or cancers among these veterans' future 
offspring. Of course, when our men and women are sent to war, their 
future fertility and the potential for birth defects are not their main 
concerns, and for many reasons, neither the Pentagon nor the 
Department of Veterans Affairs has worried about those risks, nor 
have they made any efforts to reduce those risks or spend money to 
study those risks. 

Nevertheless, many veterans are experiencing serious reproductive 
problems, and they wonder if these problems were caused by their 
military service. The first major complaints came from atomic 
veterans and Vietnam veterans exposed to Agent Orange. Both 
groups of veterans believe that military exposures caused infertility 
and birth defects. 

In recent months, similar concerns have been repeatedly — 
repeatedly — expressed by Persian Gulf veterans. All these men and 
women went to war willing to face unspeakable dangers, and, of 
course, they were willing to face death. But they never expected their 
future children to suffer. 

The purpose of today's hearing, therefore, is to listen to those 
concerns. We will hear from veterans, from their spouses and widows, 
and from scientists from across the country, including some in this 
administration. We will also be asking questions about what the 
Pentagon and the Department of Veterans Affairs have done in the 
past or are doing in the present or expect to do in the future about 
some of the questions that will be raised in the first two panels. I 
hope that we will also hear how they expect to do better in the future. 

This will be a very important hearing. I'm not sure there's been 
one exactly like this before, and this Chairman is looking forward to 
this hearing very much. 

[The prepared statement of Chairman Rockefeller appears on page 
53.] 

Chairman ROCKEFELLER. We have with us this morning Senator 
Paul Wellstone, who has been very helpful regarding this hearing. 
Although he's not a member of this Committee, he is a participant in 
this hearing, and we welcome him and any comments that he might 
have. Senator Wellstone is from Minnesota. 

OPENING STATEMENT OF SENATOR WELLSTONE 

Senator WELLSTONE. Thank you, Mr. Chairman. Your remarks 
were very eloquent, and I really appreciate the fact that you're 
holding this hearing today. I've been very anxious for us to have such 
a hearing. As you know, I've been working very closely with atomic 
vets. I'm going to get a chance to introduce Smoky Parrish, who's 
here from Minnesota. 

I guess the only thing that I can say, because I think it applies 
across the board to Gulf War, Agent Orange, and atomic vets, is that 
in some of the meetings that we had with atomic vets in Minnesota, 
Mr. Chairman, a pattern emerged of people talking about the health 
problems of their children and, in the case of atomic vets, their 
grandchildren. And I thought to myself, as a father and a grandfa- 



ther — I just had a grandson last week, a second grandchild — ^there is 
a question that just has to be answered for the men and women that 
served our country: "Could it be that in serving my country, I have 
put my children or my grandchildren in harm's way, in jeopardy? 
Could that be what has happened?" And I think that it's vital for us 
to focus on that question. It's so important for our veterans to have 
answers to the questions that they're asking. We owe it to them as a 
Nation. 

I think this hearing is extremely important, and I thank you, Mr. 
Chairman, for your help, especially in relation to some of the work 
I'm doing with the atomic veterans. I feel very good that we're going 
to really be able to do some things that are going to be important, 
that are going to be reassuring, and that are going to be responsive 
and accountable to all of you who are here today and all the people 
that you represent by being here today. 

I thank you. 

Chairman ROCKEFELLER. Thank you. Senator Wellstone, very 
much. 

I'd like to go right now to our first panel, and as I call your names, 
please come forward and sit down. 

Our first panel will include veterans and family members of 
veterans: Jackie Maxwell, the widow of an atomic veteran; Smoky 
Parrish, an atomic veteran himself; Tom Goonan, a Vietnam veteran; 
Stephen Miller, a Persian Gulf War veteran; and Kelli Albuck, the 
wife of a Persian Gulf War veteran. 

I thank you all very much for coming. I want you to know that 
these things are hard, and particularly because they're personal 
they're hard, and yet you're willing to come and speak and speak for 
others, and to help others and give others hope, because you're 
sharing with us very difficult stories. They're stories, I suspect, that 
represent the stories that many people would wish to be able to tell 
themselves. 

Now, as you know, in this atmosphere we have in Washington, 
where we have hearings, your testimony has already been submitted 
in the record and is part of the record, and we've asked each of you 
to try to keep your statements to 3 minutes. That may not be 
possible, and the Chair will be understanding on that, but that's 
simply because we're trying to complete a hearing before the early 
afternoon. But you do the best you can on that. 

And then I have to ask you, now that you've all sat down, to all 
stand up again, because it's our custom in this Committee, because 
we take our work seriously and we want what we say to be part of a 
formal national record, so to speak, that I swear in all witnesses. 
That's part of the custom of this Committee, at least, it is under me. 

So I'd ask you to stand and to raise your right hands. 

Do you swear in your testimony that you will tell the whole truth 
and nothing but the truth? 

[All witnesses respond in the affirmative.] 

Chairman ROCKEFELLER. You may be seated. 

Mrs. Maxwell, can we start with you? 



STATEMENT OF JACQUELINE C. MAXWELL, WIDOW OF 
ATOMIC VETERAN, DIRECTOR, ATOMIC PARENTS, NA- 
TIONAL ASSOCIATION OF RADIATION SURVIVORS, MENLO 
PARK,CA 

Mrs. Maxwell. I'd like to preface my remarks by giving special 
thanks to your staff, to all of you for this hearing itself — it's a dream 
come true for me — and especially to the DAV representative Dave 
Gorman, who moved heaven and earth to get me here, and to a 
special DAV rep that's been part of my life, Santon W. Lore, for at 
least the last 15 years. 

As you've mentioned, we are all here for one cause, and one cause 
alone, and it's for the birth-defected children, especially from ionizing 
radiation. I am Jackie Maxwell. I'm on the board of the National 
Association of Radiation Survivors. I'm a director of the Atomic 
Parents of Genetically Impaired Children. We have a 7,000-member 
data bank, with 20 percent of those radiation survivors children with 
some form of defect. Of the 452 veterans that we have from the 
Hiroshima/Nagasaki area, there are 107 anomaUes. These figures are 
astronomical when you think the rate in the whole population is just 
3 to 5 percent. 

My husband was one of those atomic veterans, and as this is his 
story, I'm going to introduce you to him, tell you of his background, 
and let him put faces on five of these statistics, so you're just not 
hearing numbers. 

Standing here before you is a literal giant of a man, a 6'3", 185- 
poimd, extremely handsome, charismatic and self-assiired, habitually 
happy man. He's Staff Sgt. Albert R. Maxwell of the 194th Tank 
Battalion. He entered the service in 1939, was at Clark Field until 
the bombing of Pearl Harbor, and then went to the defense of Bataan. 

He survived the Bataan death march and was beaten, tortured in 
camps from Santo Thomas, Cabantuan, O'Donnell, Bilibid Prison, 
Santo Domingo, Mukden, China, and survived one of the Maru 
Hellship sinkings. There were 1,500 of our POW's on that ship, and 
the ship was unmarked, and so the ship was sunk by one of our own 
subs. He was one of 55 that survived. He was first, last, and always 
a survivor, and that's what he thought of himself as. 

The final 2 years of his imprisonment were spent at one of 
Nagoya's concentration camps. There were 12 such camps from 
Nagoya, at the point of the city, to Hiroshima, which was almost the 
apex of the atomic bomb. Their camp was located along the shoreline, 
and he was in Camp 6, which they thought was almost halfway 
between these two points. 

The naval ships had been bombing the coastline for quite some 
time, and early this one morning they felt the reverberation aU along 
the shoreline, heard this tremendous boom, thought it was another 
one of the bombings, went out and saw the mushroom cloud. They 
witnessed the mushroom cloud. Shortly thereafter, there was this 
dirty black storm, they thought, which, of course, was the black rain 
and the fallout. 

Three days later — because of his size, he was always detailed to 
the largest cleanup details — he was detailed somewhere in northern 
Honshu province, and it took them almost 14 hours to get there. They 



didn't know that they were on the outskirts of Hiroshima, and he 
wrote in his diary, "Nothing I've ever read or heard of could quahfy 
as an explanation for this destruction." He said, "The devastation is 
terrible. It can't have been any national disaster nor bombing nor 
phenomena," and he noted in his diary that he had seen outlines of 
the figure — ^he thought it was outlines of the figures on the grounds, 
on sides of buildings. He didn't know at the time it was the figure 
that was burned into it. 

They were there for 3 days — three different work details for 3 days. 
They had no protective gear. They had half a cup of rice, which was 
all tiieir allotment for a day, and water, which they ingested fi-om one 
of the several rivers surrounding the city, and, of course, they were 
polluted. When they finished with it, 18 of them had this tremendous 
rash, etiology unknown — ^the/ve never been able to determine what 
it is — ^where the skin raises just like you've placed a waffle iron on it. 

His camp was the very last of the prison camps to be liberated 
from September 2 to September 9, and they were picked up by the 
USS hospital ship Hope, which went along the shoreline picking all 
the other prisoners up and bringing them home. 

Al arrived on November 15, 1945, in San Francisco. He weighed 89 
pounds. Upon returning home, he wanted to reenlist in the service, 
but his excellent physical condition had deteriorated due to extreme 
malnutrition, amoebic dysentery. Dengue fever, malaria, ravages of 
extreme malnutrition, violent headaches, constant nightmares, edema 
of the extremities, residuals of beri-beri (wet and dry), which now 
finally has been recognized as a factor in ischemic heart disease and 
is service connected. We met and married 13 months later. 

The following are excerpts fi'om Al's diary. I did not even know of 
its existence until 35 years later, when he needed it for a claim. 

I have to thank the ABDC [Association of Birth Defect Children] 
group for this, because the actual diary has been stored with all my 
possessions for 5 years. I couldn't get to it. And I have to apologize, 
because there are mistakes here, £ind I didn't have time to proofread 
it. 

He said, "Wonderful news." This is December 1947. "I'm no longer 
sterile. How about that? And we are expecting a baby." I don't think 
either of us was ever so happy. 

"We have the most beautiful baby girl. Lots of black hair, enor- 
mous, big blue eyes, and dimples, 6 pounds, 7 ounces. We named her 
Paulette, after Jackie's mom. 

"Our baby has a rare heart abnormality called tetralogy of Fallot, 
a condition of foiu* concurrent problems with the heart wherein each 
chamber of the heart has a different heart deformity. She also had a 
misplaced rectum and premature showings of hydrocephalus, which 
they have corrected surgically. They told us she probably won't live 
much longer than a year. 

"They've certainly put us through the wringer with questions about 
have we had any radiation exposure? Had [Jackie] undergone X-rays 
when she was pregnant? Did she have dental work done? None of the 
above. 

"Our baby is really a daddy's girl. She dimples every time I even 
look at her and gets so excited when I walk toward her that she 



6 

hiccoughs. When I pick her up, she chuckles out loud, only 3 months 
old. Has a tooth at this age. She has my whole heart in those tiny 
hands." 

I watched this giant of a man who kept his feelings bottled up just 
open up to her like a flower to the sun. 

"Paulette has filled our whole life with joy. She's such a charmer 
with those smiles and dimples and a very happy, siuiny disposition. 
A real giggler. She's so dainty. I call her 'Star Eyes.' 

"September 1949. We've lost our baby. I'm so desolate. She was ill 
one day and gone the next. Try to think of it as a blessing for her 
sake, so she won't have to suffer, but all I can think of is she's gone. 
This pain surpasses anything I've ever endured. 

"Sick. Nightmares. I haven't slept since Paulette died. I've lost 20 
pounds. 

"February 1950. We're going to have another baby. This time they 
will take it cesarean. 

"June 14. Baby boy. Husky little guy. Three blonde hairs on his 
head. Where did they come from? Weighs 8 poimds, 10 ounces. Name 
Michael Birch Maxwell. 

"Against impossible odds, this baby has tetralogy of Fallot also. 
Doctors say they've never known such an occurrence. We're stunned. 
They've come fi-om all over the western States to examine both of us 
and Michael and Paulette's medical records, trjdng to determine the 
cause. We questioned all members of both sides of our family." 

He was the youngest of seven children who produced some 52 
offspring, all of them normal; 52 grandchildren, likewise. In my own 
history, we had gone back in our genealogy at least 200 years — no 
abnormalities, and I lived with a grandfather, a great-grandfather, 
and a great-great-grandfather who lived to be 104. So I knew pretty 
much what we had in our families. 

"June 1950. Some hope. He has an otherwise healthy body. They 
tell us, 'Try not to give up hope. We'll try to prolong his life.' " That's 
what they always tell you as a doctor, "Wait, prolong his life, and 
there will be an operation." 

"They've been monitoring Mikie carefully and discovered that he 
also has premature showings of hydrocephalus. They are going to 
operate on him, remove a kidney, insert a catheter, and drain off the 
excess fluid. It's so risky because of his heart. 

"The operation is a complete success. They're showing films of it at 
the Boston Medical Convention." They showed these same films for 
35 years. "Mikie will be hospitalized for 3 months. I've gotten a night 
job" — this was his third job— "to supplement our income. He's going 
to have the best care possible. 

"July 1951. We have another baby girl. Not planned. A perfect baby 
girl, perfect heart, the most gorgeous baby I've ever seen. The whole 
hospital thinks so. Poor Jackie. The doctors have come in to examine 
her again. This must be 222, at least. They are all so thrilled for us, 
as she is such a doll. She has little dark curls, big dark eyes, and 
dimples all over her body. Eighteen inches long, 5 pounds, 14 ounces, 
but she's really chubby. We're all on cloud 9." This was on July 2. 

"July 4. Our perfect baby girl died today. Doctors were all stunned. 
She developed breathing problems, and quite literaUy we watched her 



smother to death. Diagnosis: atelectasis of the lungs, another 
congenital abnormality usually associated with premature birth. She 
was a full-term baby." He says, "God, she fought so hard to live. Let 
her sleep well. Your daddy loves you, little girl. 

"July 1951. I've been so bitter and so full of hurt and pain. If it 
weren't for Jackie and Mikie, I really wouldn't want to Uve. I always 
thought life and surviving was the most precious thing to come by. I 
never thought I'd feel this way, but I do. My heart feels like it's being 
ripped right out of my chest. 

"We've spent 2 full days going over all the records. The doctors are 
baffled. They said there's no previous medical history on either side, 
that it was just one of those things." 

'Tou each have a possible black gene, and when those black genes 
come together, that's what produces the abnormalities." That's what 
they told us in 1951, all except my family physician. He called Al in, 
and he sat and talked to us for about 20 minutes or 30 minutes, and 
he said, "I know all about Jackie. I don't know all about you, except 
for your Rh. You look healthy. Tell me about your background." 

When he found out that Al had been over in Japan when the 
atomic bomb was dropped, he said, "Were you anywhere near it?" and 
Al said, "Well, yes, we went in and cleaned up." He said, "Did you 
have protective gear?" He said, "No." "Did you ingest anything?" 
"Yes." He had eaten his half a cup of rice and drank the water. Our 
doctor leaned back in his chair, and he said, "Well, there you have it." 
Al said, "What do you mean, there we have it?" He said, "If you two 
were to have 10 children, 9 of them would have abnormalities." 

I said, "What makes you come to a conclusion like that?" and he 
said, "I'll give you a little illustration. When I went to medical school, 
there were seven of us from the western States that went together. 
When it came time for our radiology instruction, I had mononucleosis. 
I couldn't go. The other six did." He said, "They had an accident in 
the radiation lab while they were taking their training. Within 8 
years, six of the men had died. By the 10th year, all seven were gone. 
Four of them had children with anomalies." 

He said, "If an accident in a radiation lab can cause this, you've 
opened up a can of nightmares." He said, "I would strongly advise you 
not to have any more [children], but you're going to want to, so go to 
the rest of the medical world." We did. He was 1 percent, in 1951, of 
the medical community that believed in what today we know exists, 
ionizing radiation. 

"They did the catheterization on Mikie" — he lived 5 years — "prior 
to operating on him in September. They told us he'd never walk, he'd 
never talk, he'd never sit up. He did all of the above, and he had 
learned to swim 2 weeks before. We really fluctuated concerning the 
heart, but decided to go ahead with it. 

"He was ill yesterday. He's gone today. He never got a chance at 
the operation. He had beaten all the odds in cases like his for 
longevity, progress, et cetera. We tried never to get our hopes up for 
his future, but we fought so long and hard to give him his chance." 

This is 1956. "Jackie and I had the only serious quarrel of our 
entire married life," and I can swear that's true. "She wants another 
baby. I don't. Her doctor doesn't want her to even consider it. Said 



8 

he'd told her he wouldn't take care of her if she did, that maybe she 
could go through it again, but he couldn't. 

"Jackie's convinced both me and the doctor to go ahead." This was 
Albert in 1956. "I guess if she has that much faith, we should all go 
ahead with her. The doctor worries about a possible rupture, but is 
going to go ahead with it an3rway. She's going to try and carry the 
baby for 10 months. 

"January 1957. Robyn Kelly Maxwell has arrived. Doctors all love 
my wife. They think she has a beautiful spirit. They call our new 
little girl 'Beauty's Beauty.' She was 2 days shy of 10 months and 
weighed a whopping 10 pounds. Looks like a 2-month-old baby. 
They've run every conceivable test on her. Everything is normal. 
She's darling. Blue-blue eyes, red-gold hair, and healthy, and all ours. 
My cup runneth over. I'll have to listen to T told you so' the rest of 
my life. And to think I didn't want another baby. Thank God for her. 

"Robyn has been so beautifully healthy, we've decided to try again. 
Another beautiful dark-haired baby girl." I was unable to carry the 10 
months, and the baby was premature by 2 weeks. "Weighed 5 
pounds" — this says 10, but it was 15 ounces. "Lived the same amount 
of time as Michele. Died with the same ailment, atelectasis of the 
lungs. Her name was — ^is Rebecca. We know well see you again. Don't 
forget us. We won't forget you." 

After that, I had a miscarriage at almost 6 months. It was such a 
radical miscarriage, the fetus was so disintegrated, they couldn't even 
tell what the gender was on it. So, of course, we didn't try again. I 
had one child out of six pregnancies and out of five live births. 

We are now informed and believers. We've made a commitment to 
each other to work as long as it takes to get the Government to 
recognize the horrors of ionizing radiation upon all who are touched 
by it, specifically the unborn, as the disastrous effects on the 
reproductive system are incalculable. 

Whatever you may have heard or believe, any of you in this room, 
there is no safe radiation level. It's like being a little bit pregnant. 
You either are or you're not. 

This man was a man among men of intelligence and charm. He 
had a great belief that every Ufe has a purpose and meaning and that 
it was always worth living. In the 40 years we were married, I never 
knew him to ever slander another human being or ever tell a he. He's 
had many articles and books dedicated to him as the "Gentle Giant." 

Just prior to his death, our daughter Robyn was venting her 
justifiable anger at the Government for calling her father a liar in 
where he was in the prison camp and not acknowledging his being a 
radiation victim — in general, railing against this country and its 
injustice. He sat up in bed and said, "Don't you ever let me hear you 
say anything like that again. Our Constitution is divinely inspired. 
Don't you ever forget that. Granted, there are officials and adminis- 
trators who are inept and misguided, but if you were to find yourself 
in any other country in this world, even as an invited guest, when 
you got home, you'd get down and kiss the ground of this country and 
never want to leave it again." 

Our daughter was openly sobbing by then and said, "But look what 
the exposure has done to you and Mom, and now you're dying, and 



they still don't believe you. It's not worth it." He said, "Honey, the 
truth will always out. It may take time, but it will. As long as you 
believe in your old dad, that's all that's important. If my life hadn't 
evolved the way it did, I wouldn't have had you nor the children. I'd 
never have met your mom. You still think it wasn't worth it?" 

Thank you for this opportunity to keep my pledge to the most 
wonderful man I've ever known. He suffered agonizingly and has 
waited a long, long time for the acknowledgement of such a hearing 
to occur. I want to show you, at 60 this man was dying of cancer. He 
looked 80 years old. 

Whatever you may accomplish as a result of these hearings, the yet 
unborn will have cause to bless your name. Thank you for listening 
with your hearts to some of the real people behind some of the 
statistics. If ever I can be of assistance, please advise. 

Thank you all. 

[The prepared statement of Mrs. Maxwell appears on page 139.] 

Chairman ROCKEFELLER. Mrs. Maxwell, thank you very, very 
much. That was very powerful testimony. 

Mr. Parrish, if you're ready, sir. 

STATEMENT OF ALBERT G. "SMOKY^ PARRISH, ATOMIC 
VETERAN, MAYOR, HACKENSACK, MN 

Mr. Parrish. Yes, sir. My name is Albert Parrish, and I'm the 
mayor of a little town in northern Minnesota, Hackensack, and I'm 
a proud member of the American Legion Club, Post 202. I'm president 
of the Lion's Club there. I'm very active, and I feel that I'm a good 
American person. 

I want to thank you, Senator Rockefeller, and the panel for hearing 
us today. I guess after 42 years, it's really an honor to be here, to be 
able to speak in a country where the law says we're able to. 

I want to thank Senator Wellstone. He's from my home State, and 
without his concern and commitment, I wouldn't be here today. I feel 
very honored for that. 

I come to share the experiences that I've had and recommendations 
of what I feel that I'd like to see. I come from a little group that we 
formed about 2 months ago or 3 months ago. After Secretary O'Leary 
opened the files, we formed this little group of the company that I 
was with. In March 1952, we were ordered to go to Las Vegas or to 
Mercury, NV, to undergo eight atomic bomb tests. We were instru- 
mental in finding the radiation in the fallout, and also at ground zero, 
we had to monitor that. 

I feel that the U.S. military and the Atomic Energy Commission 
did a really poor job of protecting us fi-om the high levels of radiation. 
The first atomic bomb was detonated within 8 miles of the camp we 
lived in. We lived there for 3!/2 months. The other seven were 
detonated 50 miles away. 

If I had time, I'd tell you what the living conditions were like. They 
had plywood huts, plywood roofs, no roofing, no windows, and 8 miles 
from the first ground zero, and the water cost 7 cents a gallon, so 
they didn't allow us any water to scrub the huts out. I've got a letter 
written in March 1952 in my files that says that, a letter I wrote to 
my mother at the time. 



10 

Before I went to Nevada, I had one normal, good child. That was 
in November 1951. In March 1952, when I went out there, after that 
we lost three stillborn children, and had two miscarriages, and the 
doctor told me that I either had to stop trying to have children or my 
wife maybe couldn't handle it because of her emotional and physical 
condition from trying to have another child. I have the footprints of 
one little boy in my briefcase, but I didn't take it out. 

Then, after the stillbirths, I had problems. I had a tumor on one 
testicle. I had to have the tumor removed and then consequently had 
to have a vasectomy. But that really didn't bother me, because we 
really couldn't afford to take a chance with my wife's life anyhow 
after that. So the tumor and the vasectomy didn't bother me too bad. 

In my written statement, I have four recommendations that I'd like 
to see implemented. I'd like to read one of them. I know we don't have 
time to read them all, so I'd like to urge the Committee strongly to 
consider funding a comprehensive independent study to examine 
health effects for family members of atomic veterans, and then, based 
upon the results of that study, take appropriate action to care for and 
compensate our atomic veterans and their families. 

I first asked — and I have that in the written record also — in 1958, 
January 1958, while I was having all these problems, I went to the 
Department of Veterans Affairs, and, of course, they're held account- 
able under laws, and I just didn't fit in. I asked to get in and have a 
physical, and they said, "We can't give you a physical unless you file 
a claim." I said, "Well, I just wanted a physical." And it's in writing. 
I've got it right here. They said, "We can't give you a physical, 
because you haven't filed a claim," and I said, "I don't want to file a 
claim. I just want a physical. I just want to find out what's the 
matter," and they said, "We're sorry." 

So I filed a claim, and then they said in one sentence, "We're not 
concerned about you. You filed a claim, and we're not concerned about 
that, because your claim is invalid." You see, they said that the 
amount of radiation — they keep saying that, "You didn't have enough 
radiation. It doesn't matter how much radiation you had, it just 
wasn't enough." 

So I'd like to cut my message off. I have 42 years of things to say, 
so it's kind of hard for me to quit. But I appreciate the time that 
you've given me. I will thank you and ask for any questions — 

Chairman ROCKEFELLER. You had four recommendations you were 
going to— 

Mr. Parrish. Yes, I do, and they're in the record. Would you like 
to hear them? 

Chairman ROCKEFELLER. Yes, why don't you give them to us. 

Mr. Parrish. All right. 

Senator WELLSTO^fE. Mr. Chairman, while Smoky is going through 
his briefcase to get the recommendations, I'd like to thanlk you for 
permitting him to read them. Smoky came all the way from Minne- 
sota, so I really appreciate that you have given him this opportunity. 

Mr. Parrish. The first recommendation is — and I've read 
that — immediately fund a comprehensive independent study to 
examine the health effects and consequences for family members of 
atomic veterans of exposure to ionizing radiation. I understand that 



11 

this request has been made by atomic veterans at several congressio- 
nal hearings in the past. 

Number 2, to take immediate and appropriate action to service 
connect and compensate atomic veterans and family members for 
reproductive problems. Of course, this type of action would have to be 
contingent upon the results of a scientific study. 

Number 3, to continue to examine all health-related problems 
linked to radiation exposure and expand the Ust of radiogenic service- 
connected conditions, where appropriate. 

Number 4, to ensure atomic veterans receive all relevant documen- 
tation and materials needed to support claims for veterans' benefits, 
including more accurate reconstructed dosage amounts. If need be, 
give the veteran exposed to radiation the benefit of the doubt and 
presume that the veteran was exposed to unsafe levels of radiation. 

And I can add to that where I feel that the amount of radiation 
was not accurate, and I feel that I'm a person that can vouch for that 
in a short story, in a 2-minute or a minute longer thing, where I 
know — well, let me try and do it in about 30 seconds. 

I was sent out one day to evacuate a mine. I was on the Radiation 
Safety Committee, and there were 196 people. One hundred thirty- 
four of them were fi*om our outfit, and almost 100 of them from 
Minnesota. So we're thankful to have Paul Wellstone, because hell 
listen. I was sent out to a mine and had to evacuate the mine, and 
while I was evacuating it, I knew the miner, and I drank a glass of 
water, and he said, "You didn't drink that water, did you?," and I 
said, 'Tes." He said, "Our tank is open on the top, and every time 
that we get a shot coming this way, we have to clean it out." 

So I got the instrument. The shot was on a tower. It disintegrated 
a 300-foot tower, went out into the fallout, came down, and, sure 
enough, the specs were in my hand. I tested it with a Geiger coimter. 
It was hot, but I'd already drank the water. I didn't feel too bad until 
40 years later, and I called Mr. Wellstone's office, and I said, "I don't 
want you to believe me, but would you believe all of the guys in our 
outfit? I can write to a few of them." He said, 'Tes." 

So I wrote to the fellows, figured, well, $29 for stamps, and so I 
wrote to the fellows, and some of them came through, and they 
returned letters to me. I read this one, and I don't want to read it 
today because it's so emotional, but after I had evacuated a mine 
from the civilians, they sent my friend in, and he had to stay there 
for 3 weeks and take filters out of an air filter machine and meet the 
helicopter so they could take them back to see how much radiation 
was in the mine area. About 40 years later, I found out that he's been 
paralyzed half his hfe. He's had a tumor inside of his spine, and they 
operated on him. He lost his business, he lives on Social Security 
disability. 

I've got another fi^end that had six children. The first one was bom 
live. The second one died. The third one died. The fourth one was 
bom alive. So he had two out of four. The fifth one died. So he had 
lost three. The sixth one was bom premature, and the child was a 
paranoid schizophrenic. 

I sent out letters, and I got 45 letters in return fi-om the letters 
that I sent out, and I asked my buddies to fill out what they had 



12 

wrong with them — ear problems, nose problems. Fifteen out of the 45 
had reproductive problems. So it's a common thing, and I just feel like 
I really felt good to do it. 

If you have time, I'll read you about one sentence out of this book. 
Would you have that much time? 

Chairman ROCKEFELLER. Go ahead, sir. 

Mr. Parrish. This is how we were treated, and it's not nice. This 
is out of a Government book. It's the U.S. Department of Commerce 
book. It's on page 159, and I have a photostat of it in my written 
record. It says, "Several of the overexposed personnel listed partici- 
pated in the military effects test group project that required them to 
enter the radiation areas to retrieve instruments and records. To 
complete these activities, personnel may have had to spend a 
considerable amount of time in the radiation area." 

It also says, "They were permitted to enter the shot area before the 
recovery hour, because immediate recovery of the equipment" — and 
I won't read the other words — "was important," but it was more 
important than our lives and our families and our children. I just 
don't think it was right. 

Like I say, all the questions that you have, I could answer, but I 
don't want to take any more of your time. I appreciate it. I thank you 
for what you're doing in this field so that we can be at least thankful 
before we die that we've done something for the people and keep the 
other veterans out of chemical warfare and chemical things. It's not 
right. 

Thank you, Mr. Chairman. 

[The prepared statement of Mr. Parrish appears on page 145.] 

Chairman ROCKEFELLER. Mr. Parrish, you've waited a long time to 
testify. But imderstand that when you do what you have done, that 
you're speaking for so many and you're helping so many. So that as 
hard as it might be even to contain all the things, as you said, fi-om 
42 years of memories and experiences that have not necessarily been 
very happy, you're opening doorways of possibilities for maybe 
hundreds of thousands of other Americans. So you should be very 
proud of your testimony and what you do, as should all of you. It's 
hard, and it's important. 

Mr. Goonan, when you're ready, sir, we'll be happy to hear from 
you. 

STATEMENT OF THOMAS M. GOONAN, VIETNAM VETERAN, 
ASSOCIATE DIRECTOR, AGENT ORANGE FAMILY ASSIS- 
TANCE PROGRAM, UTAH STATE UNIVERSITY, LOGAN, UT 

Mr. Goonan. Good morning, Mr. Chairman, members of the 
Committee. My name is Thomas Michael Goonan. I live in North 
Logan, UT, and I am here today because I am the husband of a 
courageous woman, the father of two children bom with birth defects, 
a Vietnam veteran, and the associate program director for the Agent 
Orange Family Assistance Program at Utah State University. This 
program is fiinded fi-om a grant by the Agent Orange Class Assis- 
tance Program. 

I served in the RepubHc of South Vietnam in 1971 and 1972, in the 
region known as IV Corps. I was stationed for the majority of my 



13 

time at 3rd Surgical Hospital (MASH) in Bihn Thuy and at Can Tho 
Air Base. During this time, my duties varied from working in the 
emergency room, working on various wards, and working as an 
assistant to a maxillofacial surgeon. 

In Bihn Thuy, there was a Navy river patrol unit, infantry, and 
engineers. The perimeter was regularly defoliated with Agent Orange, 
as were portions of the Mekong River, where we drew our drinkmg 
water. This has since been validated by one of the clients to whom I 
have provided services through my work at Utah State. His written 
statements include evidence of spra5ring as well as having a child 
with an oral cleft and learning disabilities. 

During my tour, I was a member of a team of medical personnel 
who flew missions to many MACV/Special Forces compounds 
throughout Military Region 4, as well as the POW camps located on 
Con Son and An Thoy Islands. These missions included areas that 
were defoliated by Agent Orange during the 1960's and early 1970's. 
I returned to the United States in June 1972 and was honorably 
discharged in January 1974. 

Upon my return home, I enrolled in coUege and received a bachelor 
of fine arts degree. In 1978, a woman that I was dating experienced 
a miscarriage at 8 weeks. I began to notice lesions on my shoulders, 
back, and upper arms. I had minor surgery in 1982 to remove a 
benign tumor fi-om my soft palate, and since that time, I have had 
two sebaceous cysts removed from behind my ears and a 75-gram 
lipoma removed fi-om my left shoulder, and I have another lipoma on 
my left forearm. 

In 1984, 1 moved to Utah. I met my wife, Marijane Lindley, and we 
were married in 1987. Marijane was married previously and had 
three sons fi*om that marriage. There were no complications or birth 
defects associated with any of these children. 

In 1988, our first son was bom. During the term of that pregnancy, 
Marijane developed pre-eclampsia/toxemia in her fourth month. She 
was ordered to bed by her doctor, but continued to work because our 
health insurance was through her job. Michael was bom 6 weeks 
premature, weighing 5.5 pounds. In addition, our son was bom with 
an incomplete cleft lip. He has had three corrective surgeries since his 
birth and is scheduled for a fourth surgery on August 12, 1994, 1 
week fi-om today. 

In 1989, our second son was bom 3V^ weeks premature, weighing 
7 pounds, 10 ounces. Jordan was bom with a unilateral cleft lip and 
palate. Jordan has had three corrective surgeries so far and is 
scheduled for two more before he enters the first grade, as well as 
major orthodontic work. 

When Michael was bom, Marijane and I were devastated. She was 
ill fi-om the toxemia, her blood pressure had spiked on the delivery 
table, and she and my son almost died as a result. I had never been 
as afraid of losing the most important part of my life as I was that 
day. 

I had waited a long time to have children — I was 35 when my son 
was bom — and my initial reaction to Michael's birth defect was that 
it would be better if he had died at birth. I am not proud to admit 



14 

this, but it's true. I soon realized that this small child was my son 
and I had the overwhelming responsibility of his stewardship. 

Marijane was deeply distressed by the fact that she did not bear 
me "the perfect child." Of course, she felt it was her fault. I suspected 
at that time that Michael's cleft lip was related to Agent Orange 
exposure, but I didn't speak about it. When Jordan was bom in 1989, 
I was depressed and angry. In my mind, there was no doubt that the 
birth defects could be traced back through my genetic makeup. 

We were counseled by Dr. John Carey, the head of the genetics 
department at the University of Utah, and it was determined that 
since there was no history of oral clefts on either side of our families 
back three generations, that it was entirely possible that a parent 
sperm cell could have been mutated by a dioxin exposure. 

Marijane and I did not speak of our feelings, we did not speak of 
our disappointment. We did what parents do — we provided for our 
children. There were problems finding compassionate providers. The 
people around us, including our pediatrician, told us that Michael's 
cleft was no big deal, it was all cosmetic, and it could be fixed easily. 
We had financial difficulties due to medical expenses. 

When Jordan was bom, we were told that we would do fine 
because we were pros and we'd been through it before. We were not 
fine, and neither were my stepsons. They were jealous because of the 
attention paid to the younger children. 

In January 1990, I began working for the Agent Orange Family 
Assistance Program. Since then, our program at Utah State has 
worked with 465 families and 1,097 children in six States in the 
western United States and the Navajo and Hopi Indian Reservations. 
Our in-house data indicates that 17.8 percent of the 315 spouses of 
Vietnam veterans requesting services from our program have had at 
least one miscarriage. Many have had more. Several have had as 
many as five and six. The divorce rate is high. It's 38.1 percent. 
Twenty-three of the veterans have died, four of the spouses are 
deceased, and 31 of the children are deceased. The average age of the 
children is now 16.9 years. 

In working with veteran families, I have found a large group of 
children bom with muscxiloskeletal deformities, neuro-tube deformi- 
ties, malformed urinary tracts, children bom without anal orifices or 
vaginal openings, and oral clefts. These children are bom to a number 
of families and are clustered. Some families have several children 
bom with birth defects and severe learning disabilities. The socioeco- 
nomic status varies, as does the geographic area that they're 
currently living in. The constant is the time served in Vietnam and 
the area of operation in which the veterans served. 

In working with veteran families and children with disabilities, 
there's a great void in the types and quality of services available. I 
have found that there is little or no communication, nor is there a 
cohesive referral network between, for example, the Department of 
Veterans Affairs, the Department of Health and Human Services, and 
health care providers in the private sector. 

The Agent Orange Family Assistance Program has found that the 
overwhelming burden of health care forces many families into 
indigence or bankruptcy in order to qualify for public assistance or 



15 

other needs-based medical services. This has created an inhospitable 
environment for the Vietnam veterans, and veterans in general — I 
don't want to speak specifically toward Vietnam veterans, but I 
will — ^who were treated with contempt when they returned home from 
the war. 

The health care system is inadequate in meeting the needs of 
veteran families in general. There are no means within the VA policy 
structure or other health care providers which can meet the needs of 
the family and the veteran as a unit. Referral networks are largely 
nonexistent. The services within agencies are categorized and isolated 
from each other, placing the burden of responsibility for finding and 
obtaining health care services on the patient instead of the profes- 
sional. 

The psychological impact of having children bom with birth defects 
on the entire family, particularly the mother, has not been addressed 
appropriately. How does the mother help hold the family together, 
and how are her needs met? How does a parent explain to his 6-year- 
old son when he comes home and says, "I want you to call Dr. Lindley 
and have him fix my lip so I'll be a better person"? 

Thank you for giving me this opportunity to share this story and 
my experiences with the Committee. I feel it's an honor to be here 
today as an American. 

[The prepared statement of Mr. Goonan appears on page 205.] 

Chairman ROCKEFELLER. Thank you, Mr. Goonan. I think the 
honor is ours, and not only what you say, but the way that you say 
it, I think is, again, incredibly important for the thousands of other 
people who aren't here today to testify. So I really thank you for that. 

Mr. Goonan. My pleasure. 

Chairman ROCKEFELLER. Mrs. Albuck? 

STATEMENT OF KELLI ALBUCK, WIFE OF PERSIAN GULF 
WAR VETERAN, BARREVGTON, IL 

Mrs. Albuck. This is really hard. I didn't have any clue that these 
poor people have been having to go through this for so long. 

First of all, I do want to thank you for the opportunity to be here, 
because being a spouse of a Gulf War vet is — the war has not been 
that old, and I feel like we've come a long way in such a short time, 
and particularly because we've got a lot of interest in this. So I 
definitely want to thank you. 

My name is Kelli Albuck, and I was diagnosed with Gulf War 
syndrome at the Great Lakes Naval Hospital last week. I was 
referred by their doctors to proceed to Phase II of the Department of 
Defense Gulf War protocol. That day they decided I was not eligible 
for medical attention after all. 

My husband Troy was an Airborne Ranger Infantry Officer in the 
82nd Airborne Division during Desert Shield and Desert Storm. He 
was deployed for 9 months. Currently, my husband is totally disabled 
by Gulf War syndrome. 

Soon after the return of the soldiers to Fort Bragg, I experienced 
that upon intercourse there was pain and burning. After talking with 
other officers' wives, I found they had the same experience. On post, 



16 

we jokingly refer to it as "shooting fire." It sounds fimny, but it's very, 
very painfiil. 

My first miscarriage was in December 1991. I was 3 months 
pregnant. I remember thinking, "This happens sometimes." Beginning 
in January 1992, I had to see a civihan doctor, because the mihtary 
OB/GYN staff were swamped with a 2-month backlog. I received 
treatment for severe abdominal pain, infectious vaginal discharge, 
headaches, cramping, hemorrhaging, and fever. I felt as though I was 
full of infection. I had been tested monthly for sexually transmitted 
diseases, with negative results, so the diagnosis became asexual 
pelvic inflammatory disease, which, by most doctors' accounts, is an 
oxymoron. 

I continued to see my doctor every other day because of the severe 
pain and to press him for answers. Antibiotics were ineffective, but 
the ultrasound showed cysts on my ovaries. Finally, the doctor 
decided laparoscopic surgery was needed. 

I became pregnant again in February 1992. We left the Army and 
relocated to Illinois. In the third month, I asked my civilian doctor if 
he knew of any problems connected to the Gulf War. He laughed and 
said, "Oh, no, Mrs. Albuck. If there were really any problems, the 
Department of Defense or medical journals would have released a 
notice by now." I reluctantly agreed and said, "OK." Three weeks 
later, I lost that baby. I knew something was seriously wrong, 
because my first child, bom in 1990, was and is fine by comparison. 

. During the next couple of months, I was racked with depression, 
fatigue, chronic abdominal infections, and severe pain, not to mention 
intimacy problems with my husband due to painful intercourse. My 
husband experiences painful, swollen, burning, fluid-filled lesions 
after exposure to his own semen. Sometimes these lesions are bloody 
and the size of half dollars. He has also been tested for sexually 
transmitted diseases continually, which has caused us to eye each 
other suspiciously at times, but he is clean as of last week. 

By the grace of God, we were blessed with our third pregnancy, 
which gave us Alexander, who is right here. My complications with 
this pregnancy began at 5 months. I hemorrhaged and was hospital- 
ized for 2 weeks. I recall my doctor walking into the room in full 
surgical gear to tell me if the heart rate did not climb, she would take 
the baby, and, of course, he wouldn't live. 

Alexander was bom 2 months early, weighing only 3 pounds. He 
faced the following birth problems: underdeveloped lungs, strep B 
infection, spinal meningitis, cranial hemorrhage, collapsed heart 
valve, calcium deposits in the kidneys, severe jaundice, bleeding 
ulcers, cerebral palsy, vision and hearing impairments, apnea, 
respiratory distress syndrome, and bronchial pulmonary dysplasia. 
His $500,000 lifetime limit of health coverage was exhausted in 88 
days. His first bill, which I have right here enclosed, is a keepsake: 
"Please pay this amount: $154,319" after the first week. 

He appears healthy today, but still has many problems. For 
example, I took him to the local emergency room due to an extremely 
swollen groin, with severe pain and fever. The doctor had no 
explanation and sent him home with Tylenol. This problem is 



17 

recurrent. My son has even been diagnosed with yeast infections. We 
are tired of having illnesses that do not make any sense. 

My husband and I agreed not to have any more children after the 
ordeal with Alexander. Due to Gulf War syndrome's effects, my 
husband is disabled and unable to work, so we were financially 
unable to have sterilization. I was on oral contraceptives, fitted for a 
diaphragm to be used with spermicide, and we were instructed by my 
doctors to use withdrawal to prevent pain and burning and infections 
fi-om the semen. 

I was further advised by my doctor not to have any more children 
due to my health. I had no idea when Alexander was bom that I also 
had a strep infection, and my husband, after I told him I was 
pregnant this time, let me know that he was not too happy, because 
I almost died the last time, which I had no idea. 

We were gifted with another pregnancy despite our many precau- 
tions. I have made it through 7 months with only one bout of 
hemorrhaging. I am currently seeing my OB/GYN and perinatologist 
for this baby weekly. I am also still being treated for pelvic infections. 

I have spoken to over 100 other female vets and vet spouses to 
compare tragedies. Because of the similarities, I began to ask for 
more detailed testing of this baby. We are told there are possible 
deformities with this child, too. Their concerns are that the heart is 
malformed and that there are extra digits on the left foot, so this 
baby, which we know is a boy, may begin with more problems than 
Alexander. We pray every day that I make it through with this child. 

Given the number of afflicted spouses and children, it is an obvious 
failure on the part of Congress, the Department of Defense, and the 
VA to exclude us fi-om solutions. It is imperative that you include us 
in any research to determine cause and course of treatment of Gulf 
War syndrome and, obviously, of the other afflictions, too. 

I'd like to thank you for this opportunity to speak today. I didn't 
realize how many people I would actually be hopefully helping by 
speaking today, so thank you. 

[The prepared statement of Mrs. Albuck appears on page 209.] 

Chairman ROCKEFELLER. Just a quick question, and Senator 
Wellstone and I will have questions after the panel is through. But 
when you started talking to those other women, did you do that on 
your own initiative? 

Mrs. Albuck. I had to. There is absolutely no networking that I 
have found. It just so happened I was in the press, and the women 
said, "Miscarriages? Oh, well, I've had two and three." Actually, 
they're still active duty, the women I talked to. "I go to the local 
military hospitals, and I'm high-risk pregnancy. I've lost two or three 
pregnancies. Nobody's doing anything for me." I said, "Well, you've 
got to ask, you know. You're high risk. You're losing more than one 
child." They don't know what to do. 

It's obvious that — I mean, these are active duty military officers, 
women that were in the Gulf War, that are losing two and three 
children already, and they're not being taken care of. I, for instance, 
have to go to the civilian population now and educate my doctors on 
what's been going on with me, and it's really hard. 



18 

Chairman ROCKEFELLER. Thank you, Mrs. Albuck, very, very 
much. 

Steve Miller. 

STATEMENT OF STEPHEN G. MILLER, PERSON GULF WAR 
VETERAN, SAN ANTONIO, TX 

Mr. Miller. Mr. Chairman, members of the Committee, thank you 
for allowing me to speak. Behind me, at home, and all across the 
United States are several hundred families I have a listing of, who 
have children with conditions related to my son's or very similar. 

I'd like to introduce you to Cedrick. This is my son Cedrick when 
he was bom in the intensive care unit at Wilford Hall Medical 
Center. This is my wife with him after he finally came off the life 
support. I'll read Cedrick's story to you now. 

My name is Stephen Miller, and currently I'm an active duty 
sergeant stationed at Fort Sam Houston, TX. I deployed to Operation 
Desert Storm with the 3rd Armored Division out of West Germany 
during December 1990. At the end of January 1991, I was returned 
to Germany due to a shoulder injury. Shortly after my return, we 
conceived our second child. 

In my wife's 20th week of pregnancy, an ultrasound determined 
that the baby had hydrocephalus, and a week later an amniocentesis 
was done. We were told that it would take approximately 30 days for 
the test to be completed. After a week, we were called in to do genetic 
testing on ourselves, as a chromosomal disorder had been found in 
our child, along with hydrocephalus and spina bifida. This was 
extremely devastating, since our first child was bom in March 1990 
and she had no problems. Our genetic testing results were normal, 
showing no hereditary defects. 

Shortly after this, my wife received weekly ultrasounds as we 
began to prepare for the eftects these ainomalies would have on our 
child's life. Various physicians counseled us on the effects of these 
anomalies and potential life changes this would incorporate. 

On March 1, 1992, my wife delivered our son Cedrick Miller ftill 
term. It was then that the full extent of Cedrick's problems surfaced. 
Our child was missing an eye completely, missing an ear, one side of 
his face was underdeveloped, the heart was on the right side of his 
body, his trachea and esophagus were connected, and his thumbs 
were offset. These anomaUes were present along with the hydrocepha- 
lus, spina bifida, and chromosomal defects. 

At this point, the genetics physician inquired as to what drugs my 
wife and I were using, as these anomalies could only be caused by 
chemical means or hereditary genetic defects. We asked what they 
meant, and we were told these were a very unusual combination of 
deformities. I told the physicians I was in Operation Desert Storm, 
and at this point, they were quiet. 

Our son was connected to the various pieces of life-supporting 
equipment, and a team of doctors were called in to repair Cedrick's 
tracheal-esophageal fistula, and at this point, we wanted more MRI's 
done. 

Just for a moment here, I'd like to stop. One of the things they had 
counseled us on was that approximate surgeries for my son in the 



19 

first year were going to be between 15 and 20. They had originally 
told us Cedrick would be severely retarded, possibly in a wheelchair 
for the rest of his life, receiving massive antibiotic therapy, be 
completely incontinent, and they weren't sure about his mental 
development at all. The first MRI showed lesions on the brain. 

He was on life support, and me and my wife had at one point 
decided maybe we should make him what's known as a DNR [do not 
resuscitate] . We could not conceive of a lifetime of horror and pain 
like that for a child. Through several counseling sessions with various 
physicians and conferences, we finally agreed to let them go ahead. 

Twenty days and three surgeries later, we were allowed to take 
Cedrick home, and to date Cedrick has had eight surgical proce- 
dures — 

Chairman ROCKEFELLER. Mr. Miller, do you mean you let them go 
ahead with DNR? 

Mr. Miller. The surgeries, sir. 

Chairman ROCKEFELLER. With the surgery. 

Mr. Miller. Yes, sir. 

Chairman ROCKEFELLER. Thank you. 

Mr. Miller. I'm sorry. Twenty days and three surgeries later, we 
were allowed to take Cedrick home, and to date Cedrick has had 
eight surgical procedures, along with having to be fitted with a new 
prosthetic eye once a month. He continues to be delayed in growth 
and mental development and has had feeding difficulties. These 
feeding difficulties are time consuming in that he can only tolerate 
soft foods, and Cedrick, in the past, has had fi-equent vomiting 
episodes, several times daily and nightly. Cedrick is on the borderline 
of failure to thrive because of these difficulties. 

Once a month, Cedrick's eye is removed, £ind his socket is injected 
with a gel to create a mold in order to make a casting for a new eye. 
Due to Cedrick's peritoneal shunt, he must be closely monitored for 
any changes in mental status or physiological changes, such as 
excessive sleep or projectile vomiting, which are possible indications 
of a shunt failure. This could be potentially harmful on Cedrick's 
mental development. 

Our doctors have recommended Cedrick stay out of day care 
centers to help avoid illnesses, as even a minor illness can affect his 
weight gain dramatically, which could lead to further hospitahzations. 
Currently, my son weighs 17 pounds. A short time ago, he became 
sick, and he lost close to 3 pounds, and we were about at the point of 
having to have a tube placed in his stomach to feed him. 

Prior to deployment, I received six injections. These injections were 
not documented in my medical records. Upon receipt of the py- 
ridostigmine tablets, I inquired as to what I was being given, and I 
was told these tablets were to protect us against chemical agents. I 
was not told of any potential side effects or health risks that might 
be associated with this product. While taking these tablets, I 
experienced muscle cramping, fatigue, and severe headaches to the 
point that I could not tolerate taking these tablets. I was also issued 
insect repellant containing pesticides. 

In summary, my wife and I feel that this has had a key effect on 
our son's anomalies. We believe this because prior to my deployment. 



20 

our first child was bom healthy, without any complications. My wife 
received good prenatal care in Europe and in the United States prior 
to Cedrick's delivery. Due to Cedrick's problems, my wife and I had 
ourselves genetically tested, and the results were normal. Our 
supporting documents indicate that our son's condition may be 
related to teratogenic exposure. 

This has been an increasing strain on our family and all the other 
families we know, both physically, emotionally, and financially. We 
know of many, many families who have lost most everything they 
own. A lot of famihes still on active duty have been required to 
receive assistance from the local State agencies for either food 
supplements or food stamps in order to carry them through. Some of 
the spouses have had to give up their jobs. The husbands have been 
forced — some of them are taking on two jobs to make ends meet. It's 
very upsetting, sir. 

Thank you all for allowing me to speak. I have one letter here. I 
spoke to the gentleman last night. I gave this letter to Dr. Zuckerman 
and Dr. Olson the other day. Originally, he had asked me to wait 
until he was off active duty to read this, but 111 delete his name and 
the medical center that he's fi-om. 

I have been requested by Sgt. Steve Miller to write a state- 
ment on any knowledge or experiences I have had concerning 
birth anomalies or defects that have occurred with members of 
our Armed Forces following Operation Desert Shield/Desert 
Storm. It was with reluctance Sgt. Miller asked me to write this, 
as I'm still on active duty, and he expressed great concern 
because of possible reprisals, both subtle and not so subtle, that 
could occur to me with this statement. 

Following my deployment to Southwest Asia, I was reassigned 
to [blank] Hospital Medical Center, where my duties included 
working in the neonatal intensive care unit. Over a period of 
approximately a year and a half, I noticed an increase in the 
number of babies bom with various birth defects. This was also 
confirmed by other health care providers and nursing personnel 
who had been stationed at this location for a number of years. 

In every case that I know of involving active duty parents, 
either one or both had been assigned to a unit that served in the 
Persian Gulf during Desert Shield/Desert Storm. Although the 
direct cause of these birth defects is not known, it appears to 
correlate highly with the fact that these imfortunate infants 
have parents who were deployed to the Persian Gulf prior to 
their conception. 

Thank you. 

[The prepared statement of Mr. Miller appears on page 210.] 

Chairman ROCKEFELLER. Steve Miller, thank you very much. 

I want to say to the panel that Senator Wellstone just left for a 
moment, and I have to go, because we have a vote. It will take me 
approximately 7 or 8 minutes to go vote and come back. So we'll just 



21 

stand in recess for a few moments, and then we'll have questions that 
we'll want to ask you, if that's OK. 

Mrs. Maxwell. Might I say one thing? You've been Kstening to all 
of this, and you'll agree, after hstening to every one of us, we're what 
is termed by the geneticists as "MCA," multiple congenital anomaUes. 
There's not just one. If you have one, you have several. My first httle 
girl had 13, and you can see, when you have one, you have them 
continually. 

We have 2,000 birth defects delineated. Those that are caused by 
the things that you've heard today are so complex that the geneticists 
say it's a lifetime pursuit to pursue one defect in their careers. 

Chairman ROCKEFELLER. I'll be back very shortly. The hearing is 
just in recess. Please be at ease. 

[Recess.] 

Chairman ROCKEFELLER. If the hearing could come back to order, 
please. Witnesses, please take your seats. 

In thinking about this, going over to vote and coming back, it's 
almost, I think, superfluous to ask questions, because it's a come- 
down from the power of what you've said. So what I'm going to do, for 
my part, at least, is just to limit myself to one question to each of 
you. 

There are a lot of questions, and we will follow with questions, but 
I think what you said was so extraordinary and evocative and it 
moved me so much and, in the same sense, angered me, that it 
stands on its own. It doesn't need to be embellished by questions. 

But in case any of you have anything else you want to say, I 
thought I'd just ask you one question, understanding there could be 
hundreds. 

Why don't I start with you, Mrs. Maxwell. 

Mrs. Maxwell. I forgot to mention one thing. At the time our 
doctor expressed his opinion about the anomalies that would occur, 
he also said to my husband, "Right now you look fairly well in health, 
but I would promise you that within 19 years you're going to 
experience some form of cancer." Nineteen years and 1 month to the 
day, he started running a white count of 150,000, which took almost 
4 months before it came back down to normal. 

The chief of staff at the VA in Salt Lake City wrote across his 
chart, "Feel like this entire episodic disaster was caused by Al's 
exposure to atomic warfare," and those records disappeared. He had 
52 blood workups. Those 52 tests are not part of his record. We never 
could find it. He said, "I can't tell you this won't happen again. It's 
going to happen again. We don't know what it is." 

So within 6 years after that, he developed multiple myeloma, and 
the interesting thing is, multiple myeloma, of course, is to the bones 
what leukemia is to the blood. It just riddles you from the top of your 
head to the tip of your toes. It's 1/8 percent of all the cancer, and of 
the 24 people that went in on that cleanup detail at Hiroshima, 18 of 
them died of some form of cancer, 12 had multiple myeloma. 

Now, those figures are just astronomical, and I will say that we're 
representative of various age groups. Obviously, I'm the oldest one. 

I have to tell you my experience with my children was devastating, 
because I was led to the best pediatricians I could get, and we knew 



22 

she wasn't going to live. We just wanted to know with our first one 
what we could do to make her more comfortable, what we could do to 
help her, and we had the experience of going in and having this 
leading pediatrician say to us — he looked at her almost like she was 
an insect under glass, and he said, "If I were you, I'd take this to an 
institution and leave it there, forget you ever had it, and have 
another baby." 

How do you go home and tell your parents a thing like that? I was 
just appalled. This happened to us three different times. That's the 
way they approached it. They wanted to give you the shock syndrome 
so that you wouldn't hope, so that you woulchi't want to do anything 
for them. I think even these Gulf syndrome widows are experiencing 
some sort of reaction like that. 

But it's such a heartbreaking agony. It's easy to say statistics and 
figures and 2,000 birth anomalies and everything, but when you 
realize we've got those delineated, categorized, 30 percent don't fit 
any established diagnoses. They don't know. And especially with all 
of the conditions that we've mentioned here today, the ionizing 
radiation, all of the rest of the things, and Desert Storm. Nothing fits. 
And so you can see why it's such a problem. 

ThanJi you. 

Chairman ROCKEFELLER. Let me just ask one question of all of you, 
and, Steve Miller, I think I know the answer from your point. Do all 
of you have health insurance? How msiny of you do not have health 
insurance? 

Mrs. Maxwell. I've got Medicare. 

Chairman ROCKEFELLER. Mrs. Albuck, you don't? 

Mrs. Albuck. Because Alexander went over his lifetime limit of 
$500,000 within 88 days- 
Chairman Rockefeller. It just ran out. 

Mrs. Albuck. He's now on Medicaid. Actually, we're all on 
Medicaid, because my husband's unable to work as well. 

Chairman ROCKEFELLER. Getting on Medicaid, was that because 
of the condition of both of you or because of the fact that you just 
simply went broke trying to take care of — 

Mrs. Albuck. We sold everything we had. 

Chairman ROCKEFELLER. You spent down into poverty. 

Mrs. Albuck. Yes. We have nothing. And with this next baby, 
unfortunately, the taxpayers — this baby is going to be on Medicaid, 
and I just hope that there's nothing wrong with this next pregnancy, 
because it's not fair for the taxpayers to have to pay half a million 
dollars for one child when there should be a program already. You 
know, there's a reason for this, I would think, and we've had 
questions where people say, "Well, it's not fair that taxpayers are 
going to have to pay for this baby because of being on public aid and 
Medicaid and so on, because this baby could be very expensive," when 
we shouldn't have to be in this situation. 

Chairman ROCKEFELLER. I understand that. I mean, I think there's 
a certain irony in that we're discussing health care now in the 
Congress, and we're coming down to the point in the last 3 weeks or 
so, and we keep talking about those who have insurance and those 
who don't have insurance, and we talk about preexisting conditions. 



23 

Well, I don't think most of the people in the Congress have any idea 
of what you would explain you meant by preexisting conditions if you 
were to talk to them. There's sort of a brutal irony in this hearing at 
this moment in view of what you've all been through. 

Mr. Parrish, can I just ask you, sir, you mentioned that in the 
216th Chemical Service Company there were others who experienced 
reproductive problems. Could you just perhaps give me an example 
of one or two? 

Mr. Parrish. Yes, I could. The other ones that have — I've done this 
on my own, and so I don't have a very accurate way of doing 
anything, but I sent out a questionnaire to all the people that I know, 
and I said, "Tell me your health problems." Out of 45 people that 
answered — there were 48 people, but 45 of them were at the Nevada 
test site. Three of them were stationed in other stations. But out of 
the 45, there were 15 that had reproductive problems, we had 28 that 
had eye, ear, nose, and throat problems, most of it due, I think, to 
ingesting radiation; the gamma rays go on your film badge, and the 
gamma rays are collected and read, but the alpha and the beta 
particles that you ingest have nothing to do with your film badge. 

So there are problems, a terrific amount of other problems, too. But 
those are the conclusions that I came to just on that thing. I guess 
you'd say that every one of them that answered, other than the X's 
where they've passed away, every one that answered, almost every 
one of them had six or eight problems. More than one have thyroid 
problems where they have no thyroid left, and yet they can't even get 
their medication from the VA. So there are quite a few problems with 
that. 

Chairman ROCKEFELLER. I'll turn to Senator Wellstone in a 
moment. 

Mrs. Albuck, you have discussed something which Diana 
Zuckerman and you talked about, and our Committee staff have 
talked to dozens of other women who have experienced in part what 
you told us this morning about the "shooting fire," the pain of sexual 
intercourse because of something that is clearly wrong with the 
semen. This is not something that most of the American public knows 
about or is aware of, but it is a stunning, shocking consequence which 
is almost beyond comprehension. Do you have some friends that — 

Mrs. Albuck. Right after the men and women got home fi"om the 
Gulf War, there were, like I said, rumors. I experienced it before I 
heard the rumors. We were having problems firsthand, and I laughed 
when one of my friends said, "It's like shooting fire. It feels like fire." 
And I've wondered why or if anyone has tested the men's semen. I 
don't know what kind of test you can do. I'm not knowledgeable in 
that field. But there's got to be something that can be done. It's 
affecting marriages, it's affecting relationships. 

I've heard all of this firsthand from friends and family members, 
and all over the world — I mean, all over the United States, from 
Hawaii to Texas to Colorado, not just in my State where I reside. It's 
ever5^where. 

Chairman ROCKEFELLER. What I'm wondering is if it can cause a 
rash or a sore to develop on a man or woman's leg, what would it do 
to the inside of a woman's body? I mean, it's just — 



24 

Mrs. Albuck. Exactly. It feels like it does — all I know is that I feel 
like I'm on fire. I feel like I'm burning inside, and soon after, I get 
complete infections, just chronic infections one after another. When 
it gets on my skin, it bums me, too. 

I've had actual tests of lesions, and there's no herpes. I have 
nothing. I'm absolutely fine. I just have chronic bacterial infections. 
As a matter of fact, the bacterial infections are so strong, they have 
to keep changing antibiotics on me. It's not just, "Well, put her on C- 
Chlor or some kind of antibiotic." It's continual changing of medica- 
tion due to these — I don't get the lesions as bad as my husband, but 
the lesions shouldn't — ^from his own semen, he should not be getting 
bums. So, I mean, it's just worth testing. It's obvious. 

Chairman ROCKEFELLER. It certainly is. 

Senator Wellstone? 

Senator WELLSTONE. Thank you, Mr. Chairman. I'm going to try 
to be very brief. 

First of all, the fact that I don't ask a question of each and every 
one of you does not mean that I don't care deeply about what you 
said, and, Mr. Miller, I really apologize. I had to leave in the middle 
of your testimony. I felt terrible. We had a vote, and I had to actually 
get there a little early for this vote. I really take seriously what you 
had to say. 

I have not been in the Senate as long as Senator Rockefeller or 
Senator Daschle, but I have not, in the years I've been in the Senate, 
ever heard more powerful testimony. The one thing that those of us 
in the Senate have to do is to make siu-e that there is followup and 
followthrough so that all the people you spoke for and what you said 
ends up really meaning something. I really am very impressed with 
your testimony. 

When I talked with Smoky and other atomic veterans, no one ever 
said, "Well, when it comes to Agent Orange or Vietnam, or when it 
comes to the Persian Gulf veterans, we're not interested. What about 
us?" And I haven't heard that from any of you. No one said, "Our 
claim is more important than anybody else's." 

It seems to me, however, that we don't know what we don't want 
to know. We don't study what we don't want to study. And I think if 
there's anything that you're saying — and, of course, I got started on 
this, and I'm working with both the Chairman and Senator Daschle 
on atomic veterans — but I feel strongly that we ought to really have 
independent scientific work done. That, at the very minimum, has to 
be done. 

And I would thank each and every one of you. Mayor Parrish, I 
won't put questions to you, because we have talked about this, and 
we'll let other people have an opportunity. I thank each and every one 
of you, and I am absolutely committed to helping you. I started off 
with atomic veterans, but now after hearing all of you, I'm ready to 
work closely with the Chairman and Senator Daschle and really make 
some things happen. 

Thank you very much. 

Chairman ROCKEFELLER. Senator Daschle, just before I turn to 
you, sir, I want to ask one more question of Kelli Albuck. 



25 

You mentioned that you were recently diagnosed as having Persian 
Gulf War syndrome, and yet, as I understand it, you are not continu- 
ing to be evaluated. 

Mrs. Albuck. Correct. 

Chairman ROCKEFELLER. And I wonder why that would be. 

Mrs. Albuck. Actually, can I — my husband explains it better. It 
has to do with his military status. 

Chairman ROCKEFELLER. Sure. 

Mr. Albuck. Sir, Troy Albuck, sir. Thank you. I am a reservist at 
this point, so under regulation, only I am eligible for care at a 
Department of Defense faciUty or a Veterans Affairs facility. So when 
I went to the Great Lakes Naval Station, there was a fantastic crew 
there that did a great job with me, and I got the best care from any 
military medical facility, even though I was from the Army, that I've 
ever gotten in my entire military career, starting 10 years ago. 

They offered to let my wife come and go through the Phase I 
evaluation. At the conclusion of that evaluation, their internal 
medicine doctor gave her a clinical diagnosis of Gulf War syndrome. 
We barely made it downstairs from that to see the coordinator, a 
fantastic lieutenant junior grade named Henry Young, who's bent 
over backwards to help us out, and he was getting in trouble because 
he had gone outside of regulation to help us and offered to let that 
military medical facility see my wife for these wounds. I really resent 
that such a good man like Lt. Young had to take heat because he did 
the right thing. I think it's wrong and inexcusable. 

My wife and I worked really hard to save my boy, and I think he 
deserves treatment, he deserves the medical attention that any 
wounded trooper would get. He's fought harder and longer than any 
paratrooper I've ever seen in my life, any ranger, any SEAL. No one 
has fought harder than this man, and I know he's a ranger, because 
he stands up even when they say he can't. 

We can't get medical attention for my wife or for my children 
because I'm a reservist. I was active duty for years. I fought Panama, 
I fought Iraq. It's just ridiculous that only if I were still on active 
duty would they qualify for medical attention for their wounds. 
Abraham Lincoln set up the VA 130 years ago to bind the Nation's 
wounds. That's a pretty clear mission statement. If I were out on the 
battlefield failing mission statements like that, I wouldn't have been 
an officer for very much longer. 

It's time for the VA to step up and fulfill their mission, complete 
their mission. The Department of Defense should follow suit. I mean, 
that's what the military medical facilities ultimately were initially 
for, was to treat combat-related wounds. These are obviously 
something from the battlefield. And the only reason I know that is 
from common sense. Find me someone else on the planet that can do 
what we can do, have these unexplainable illnesses, that wasn't 
involved with someone in the Persian Gulf, and we'll believe that it's 
not Gulf-related. But until that time, we still need to eat, and we still 
need to be treated for these wounds. 

Chairman ROCKEFELLER. I really thank you. On the way back from 
the vote that we all just had, including Senator Daschle, who I'll now 
turn to, I was mentioning the testimony of all of you to Sen. John 



26 

Glenn, who, as you know, is a distinguished mihtary person as well 
as an extraordinary human being. Sen. Glenn just said that chemical 
warfare toxins will be the atomic bomb of the fiiture. That's the great 
unknown terror that waits out there for all of us unless we do 
something about it. 

Senator Tom Daschle, who's from South Dakota, was probably 
more than anybody in this Congress responsible for getting the whole 
effort toward helping those who suffered from Agent Orange, £ind he's 
a member of this Committee. He's been at a meeting about health 
care this morning — ^he's one of the leaders in the Congress on health 
care — and so he didn't have the honor to hear all of you. 

Tom, anything you want to say? 

Senator DASCHLE. Well, thank you, Mr. Chairman. I will be very 
brief. I have a statement that I would like to make part of the record, 
and I apologize profusely for my absence this morning. As Senator 
Rockefeller indicated, we had a health-related meeting this morning, 
and I had to chair that meeting, so I wasn't able to be here. 

Chairman ROCKEFELLER. Without objection, your prepared 
statement will appear in the record. 

Senator DASCHLE. Thank you, Mr. Chairman. 

[The prepared statement of Senator Daschle appears on page 54.] 

Senator DASCHLE. Let me just say, I've heard now from a couple 
of different people what powerful testimony you all have provided and 
what a tremendous contribution you've made to our understanding. 
It just seems to me that we continue to fail to recognize in this 
country that new wars bring new wounds. We are fighting 20th 
century wars and using 18th century medicine. 

And if there is one word to describe our response to your plight, it 
is "inadequate." The word "inadequate" ought to be underscored many 
times. Inadequate research, inadequate protection, inadequate 
response. At every stage along the way, our effort to address your 
needs has been inadequate. Why we don't have adequate research is 
a question for this Committee. Why we don't have adequate protec- 
tion may be a question for the Armed Services Committee. Why we 
don't have adequate protection and response following your experi- 
ence, I simply cannot say. 

But I will tell you this. There's a growing number of Senators and 
Congressmen who are determined — determined — ^to make it adequate. 
But until we recognize that new wars bring new wounds, we simply 
cannot get the job done. 

With that, Mr. Chairman, thank you, and I apologize again. 

Chairman ROCKEFELLER. Thank you very much. Senator Daschle. 

In thanking all of you, I also want to thank Melanie Ayers and 
Judy Jacobs and the many other veterans and their wives, who have 
been so helpfiil to this Committee in gathering information not only 
for this hearing, but for the investigation, which is ongoing, which our 
staff, led by Diana Zuckerman, has been conducting for almost a year. 

In fact, if Melanie is in this audience, I wish you'd stand up. Thank 
you, Melanie, very much. 

I also want to thank all the veterans service organizations for their 
help with this hearing, and especially the DAV and the VFW and the 



27 

Agent Orange Class Assistance Program, who helped pay the travel 
expenses of some of our witnesses who came to testify today. 

And, Steve Miller, just before you depart — and this question came 
to me from John Moseman, who's the excellent minority counsel for 
this Committee — ^you indicated somebody who might be in jeopardy, 
and I just wanted to be sure that that person had plenty of protec- 
tion. 

Mr. Miller. Yes, sir. He'll be off of active duty here in about 14 
days. He's departing the service of his own accord. 

Chairman ROCKEFELLER. OK. Thank you all very, very much. 
Thank you for being here. Thank you for telling us our duty. 

Chairman ROCKEFELLER. Now, I'd like to welcome the second panel 
and ask you to please come to the table and take your seats. Our 
second panel includes scientists and doctors. I want to thank all of 
you for coming and testifying today. Your testimony will be very 
important as we attempt to determine if veterans and their families 
are harmed by reproductive hazards. 

The second panel includes Kwai-Cheung Chan from GAO; Dr. 
Maureen Paul, director of the Occupational and Environmental 
Reproductive Hazards Center at the University of Massachusetts 
Medical Center — thank you for coming down; Dr. Ellen Silbergeld, 
who is professor of epidemiology and toxicology at the University of 
Maryland Medical School; and Linda Schwartz, who is a nurse and 
a doctoral student at Yale's Department of Epidemiology and Public 
Health. 

All of your statements are in the record, and you have incredibly 
important things to say, and I'm not going to run the 3-minute clock, 
just because I don't feel like doing it, because I just don't think it is 
enough time. But try to be as concise as you possibly can, and I also 
need to swear you in, so please stand and raise your right hand. 

Do you swear in your testimony that you will tell the whole truth 
and nothing but the truth? 

[All witnesses respond in the affirmative.] 

Chairman ROCKEFELLER. Let the record show that all answered 
affirmatively. 

Dr. Paul, why don't we start with you? 

STATEMENT OF MAUREEN E. PAUL, M.D., M.P.H., DIRECTOR, 
OCCUPATIONAL AND ENVIRONMENTAL REPRODUCTIVE 
HAZARDS CENTER, UNIVERSITY OF MASSACHUSETTS 
MEDICAL CENTER, WORCESTER, MA 

Dr. Paul. I want to thank you very much for inviting me to testify 
at these important hearings. I have provided my written testimony, 
and I will try to stay within 3 minutes and just highlight some key 
points. 

As you wade through the academic credentials in that testimony, 
I just want to emphasize that my expertise derives mainly from the 
fact that I am a clinician, one of the few, if not the only physician in 
the country who is board certified in both obstetrics and gynecology 
and occupational medicine. 

As a clinician with experience caring for women and couples who 
have reproductive problems, I would like first to express my respect 



28 

for the people who testified today. These issues, as we know, Eire 
incredibly painfiil and personal, private issues, and it takes an 
incredible amount of courage to speak up publicly about them. I 
think, though, that we should never forget that the history of 
occupational medicine is replete with examples of breakthroughs that 
have been made because of the courage of people to speak up about 
health problems about which we knew very little. 

In fact, it was the courage of men, male workers who were 
employed at a pesticide formulation plant in Cahfomia in the 1970's 
who dared to speak up about their infertility, that led us to under- 
stand that men, too, can be seriously affected by reproductive hazards 
in the workplace. 

I'd like to highhght first some key points about reproductive 
hazards, and then to say a few words about the reproductive and 
developmental hazards that people face in the military. My purpose 
is to show that the issue of reproductive hazards in the military is a 
serious one, that the particular problems that the veterans talked 
about need to be taken very seriously, and that we should allocate 
resources and research into looking into these problems. 

I'd like to say first that the fi-equency of reproductive problems in 
the United States is significant, and that we don't know the causes 
of most of these disorders. In the past, when we thought about 
reproductive hazards, the image that came to mind was one of 
pregnant women taking a certain drug that would cause a birth 
defect, and we confined ourselves to thinking about reproductive 
problems as a woman's issue. 

We now know from research over the last couple of decades that 
there is a wide range of effects that can occiu- to both men and 
women, and that these can be due not only to drugs, but to agents in 
the environment and in the workplace that can affect the reproduc- 
tive system, and I'm just going to give a few examples. 

For instance, we know that sperm count and fertility in men can 
be affected by exposure to pesticides like dibromochloropropane, to 
lead, to organic solvents, to ionizing radiation. We know less about 
those effects in women, but we do know, for instance, that chemicals 
called polycyclic aromatic hydrocarbons can kill eggs in women, 
leading to an earlier menopause. 

We also know that there are hormones that carefully regulate the 
reproductive processes in men and in women, and that if you disrupt 
those hormones, you can have a number of adverse outcomes. One of 
the effects is menstrual disorders that can be seen, for example, in 
women who are exposed to high levels of stress and to some estrogen- 
like chemicals that can occur in the workplace £ind perhaps in the 
environment. 

Finally, we do know about substances that can cause birth defects 
or miscarriages through maternal exposure, but it's also very 
important to realize that there's a whole expanding area of research 
that indicates that preconception exposure to msdes may result in 
abnormal pregnancy outcomes. This is well documented in experimen- 
tal animals, and in humans we have some studies that show that 
exposure in males prior to conception may result in miscarriage in 
the wives after exposure to agents such as lead, organic mercury. 



29 

perhaps anesthetic gases, organic solvents, and some others. I would 
also like to say that there is some growing evidence that men who are 
employed in certain occupations may have an increased risk in their 
children of childhood cancers. 

The kind of effects that we're seeing don't necessarily have to 
happen just at high doses. Also, in terms of pregnancy outcomes, 
we're seeing not only problems like birth defects and miscarriages, 
but also very subtle abnormalities in behavioral and neurologic 
development that can result from exposures prior to conception or 
during pregnancy. There are very complicated mechanisms by which 
these effects may occur, and these will be addressed by other 
scientists on the panel. 

Senator Rockefeller's office asked me to review the potential 
reproductive and developmental effects associated with military 
exposures, like radiation, dioxin, 18 different pesticides, and some 
metals that were used in the Persian Gulf War, and I have done that. 
I obviously can't tell you all the effects orally, but let me just 
emphasize two things. 

One is that some of these agents — the pesticides especially — ^have 
not been well studied in humans. This is commonly the case for 
reproductive effects; for many agents, the potential reproductive 
effects have not been well studied. There has been, however, pretty 
convincing evidence of toxicity in animals for many of these agents; 
and in some cases, like radiation and lead, these have also been 
studied in humans. I was really struck by how many of these agents 
are suggestive reproductive or developmental hazards based on 
examination of the animal or human data. 

In conclusion, I would just like to emphasize that the issue of 
reproductive hazards in the military is an incredibly important one, 
that we have much to learn about reproductive hazards, but that it 
is clear from my examination that many exposures that the veterans 
had have at least the potential to cause adverse reproductive and 
developmental effects. I would urge the Committee to allocate 
resources for research so that we can identify potential hazards and 
their mechanisms of action, define better the types of problems that 
people are experiencing and how frequently they are occurring, and 
then design some sound epidemiologic studies to look for links 
between the exposures and those outcomes, and that we use both 
animal and human data to study these problems. 

Giving appropriate attention to this issue, we must remember, 
provides us with the opportunity not only to learn more about 
reproductive hazards and to respond to the needs and the concerns 
of people in the military, but also hopefully to better inform and 
protect military personnel in the future. 

Thank you. 

[The prepared statement of Dr. Paul appears on page 236.] 

Chairman ROCKEFELLER. Dr. Paul, thank you very, very much. 

Dr. Silbergeld, can we go on to you? 



83-529 95-2 



30 

STATEMENT OF ELLEN K. SILBERGELD, PH.D., PROFESSOR 
OF EPIDEMIOLOGY AND TOXICOLOGY, DEPARTMENT OF 
EPIDEMIOLOGY AND PREVENTATIVE MEDICINE, UNIVER- 
SITY OF MARYLAND SCHOOL OF MEDICINE, BALTIMORE, 
MD 

Dr. SILBERGELD. Thank you very much. I'd Hke to echo Dr. Paul's 
reactions to the testimony we've just heard. I wish, as a scientist, that 
there were some way we could say to these veterans, their families, 
and others that science and medicine could explain these events and 
could offer some hope for healing and for prevention. But in fact, in 
many respects, we cannot. 

However, I think one of the greatest benefits of this hearing and 
one of the most positive outcomes that could result would be if we 
place ourselves and the scientific and medical community within the 
Department of Defense, the VA, and outside in a position to be able 
to answer £ind to help in the future, or else we will be, as Senator 
Daschle said, in the same place, confronting new wounds as a 
consequence of new wars, with no new help or information to assist. 

I'd like to focus, in my summary of my testimony, on some 
perspectives I draw fi-om my own research and that of others on the 
cutting edge of reproductive biology and toxicology which really relate 
to understanding the ways in which paternal exposure — that is, 
exposure of men — can affect the growth and development of their 
children. I think it's important to discuss this issue, because it is 
extremely significant for evaluating the reproductive risks of 
exposures of men who have been in military service, and it is the area 
in which we know the least. 

Until recently, in fact, scientists and nonscientists alike have held 
a rather limited view of the importance of fathers in reproduction and 
development. We obviously understand that the father is important 
in human reproduction for initiating the process, but we've generally 
thought that after donating genetic material at the point of fertiliza- 
tion, fathers play little or no role in determining the outcome of 
reproduction — that is, the growth of the early embryo, the fetus, and 
the postnatal fate and development of the infant. 

Because we assumed this, we therefore assumed that men couldn't 
really contribute much damage to reproductive outcomes, that the 
greatest risk and the thing we really had to look for was to examine 
reductions in fertility or perhaps serious and specific birth defects as 
the only endpoints that could plausibly be associated with exposure 
of fathers. 

And we also have assumed that since sperm are constantly being 
recruited, there was little or no possibility of long-term or delayed 
damage — that is, if the father were exposed through military service, 
occupation, or other situations to a toxic chemical that 2 or 3 years 
later, there would be no toxic sequelae that could be associated with 
that exposure. 

Some persons have also suggested that there's some kind of 
natural selection of the fittest such that damaged sperm from men 
are not able to compete for fertilization of the egg during conception 
and, therefore, it would be impossible for the male to contribute much 
in the way of damage. 



31 

Now we have recognized that there are at least two ways in which 
exposures of men during the period of conception can be transmitted 
and affect the fate and development of the embryo, fetus, and infant. 
We have known for some time, for instance, that impairments in 
reproduction that we've observed £ifter exposure to anti-cancer drugs, 
such as cyclophosphamide, or the abuse of alcohol and cocaine are 
associated with the actual appearance of those chemicals in seminal 
fluid. So, in essence, the father becomes the route of exposure of the 
mother at the time of conception. And we've also been aware that 
there are certain hereditary and acquired birth defects, mutations 
that are passed by the father at the moment of genetic combination 
of the father and mother's genome at fertilization. 

But we now understand that fathers play a much more complex 
and influential role in early development of children. Fathers provide 
at conception not only half the genetic material of the new organism 
of the child, but many other factors contained in sperm and seminal 
fluid that we recognize are important regulators of very early cell 
division of the fertilized oocyte, the successful implantation of that 
fertilized oocyte, and the critical stages of early embryonic develop- 
ment. 

As we recognize these new significant factors contributed by the 
father, we. have to recognize that there are additional opportunities 
for adverse influences to take place as a result of the father's 
exposures. 

In addition, we now understand that it sometimes matters very 
much from which parent you inherit a specific gene. This is the 
concept of genomic imprinting, and we know this plays a role in 
major diseases, such as some of the retinoblastomas, Huntington's 
disease, and Wilm's tumor. The fact that this occurs means, of course, 
that the notion that somehow only the fittest sperm survive to 
fertilize the egg cannot be true. 

There are a number of reviews, including Dr. Paul's recent 
publication, on occupational and environmental exposures to 
reproductive hazards which summarize what we know about the 
potential toxic effects to men and their children resulting from 
chemical exposures, but, in fact, very few agents have actually been 
studied in terms of their possible effects on the growth and develop- 
ment of children fathered by exposed men. 

Epidemiologically, some of the strongest evidence that exists 
associates paternal exposures to lead and cadmium with reduced 
fertility and also increased risks of miscarriage and, later, neuro- 
developmental defects in children. And from our studies on lead 
particularly, we have some understanding of some of the mechanisms 
that may be critical to study in some of these other conditions, 
including the situations involved in the veterans' exposures. 

For instance, chemicals like lead can appear in seminal fluid, and 
their concentrations are related to the exposure of the father. Thus, 
there can be direct exposure of the sperm and oocyte at the moment 
of fertilization. In addition, we know that lead, dioxin, and a number 
of other chemicals afl"ect aspects of the neuroendocrine axis, for 
instance, in men, affecting the balance between circulating levels of 
hormones such as LHRH and FSH, and these have effects on 



32 

decreased sperm count, motility of sperm, and the ability of sperm to 
actually penetrate the oocyte and fertilize the egg. 

But we also know from animal studies that doses of lead that do 
not affect fertility do significantly affect the early development of the 
embryo and fetuses fathered by lead-exposed males. We understand 
now that these effects can occur through nongenetic means and they 
may, in fact, represent stable effects occurring as a consequence of 
preconception exposure significantly before animals mate. 

So we must conclude, in fact, that toxic substances can affect male 
reproduction, that these effects occur in ways other than reducing 
fertility, that many of these effects, in fact, may occur at doses lower 
than those that cause infertility or subfertility, and that these 
exposures may produce long-lasting effects in children fathered by 
exposed males. 

Now, if I may conclude by saying that the reason why we know so 
little, and the area in which I believe you can do the most. Senator, 
in terms of changing this situation, lies in three respects. First, the 
first research need is simply more and better testing of suspect 
agents. As Dr. Farland from the EPA, who, I think, will follow us, can 
tell you, the amoimt of knowledge that we currently have about 
chemicals used in military theaters, in the workplace, and present in 
the environment and our food supply related to potential reproductive 
and developmental effects is very, very sparse. 

Moreover, as we increase the knowledge base that we have in order 
to make reasonable decisions about human exposures to control risks, 
we need to ensure that our knowledge includes comprehensive 
evaluation of all endpoints related to male reproduction and the 
development of the offspring of males. This is not the current design 
of EPA toxicity testing. It's also very important to use experimental 
studies to determine the critical issue of reversibility or persistence 
of any effects on male reproductive function and offspring. 

With respect to the military exposures, we need much more 
information on characterizing the types of exposures that have 
occurred to the identified reproductive and developmental toxicants 
that Dr. Paul referred to and to other potentially toxic materials. We 
need to consider the establishment and maintenance of surveillance 
mechanisms which provide continuing foUowup of both health status 
and markers of exposure in the near and the long term. 

But I must conclude by saying that, in my opinion, one of the 
greatest needs is in support of basic research. Without better 
understanding of how toxic substances can affect men and their 
children, we will never be able to identify and characterize potentially 
toxic agents prior to human exposure, nor will we be able to detect 
specific adverse effects in exposed populations. Only by deploying and 
continuing to develop new knowledge in molecular genetics and 
developmental biology will we be able to inform sensitive and 
responsive epidemiologic and clinical research which will allow us to 
examine outcomes under conditions where paternal functions and the 
father's contributions to development may be at risk. 

Thank you again for accepting my invited testimony. It is indeed 
an honor to appear here. 

[The prepared statement of Dr. Silbergeld appears on page 243.] 



33 

Chairman ROCKEFELLER. Thank you, Dr. Silbergeld, very much, 
and we'll have questions for you, but now we'll go on to Ms. Linda 
Schwartz. 

STATEMENT OF LINDA SPOONSTER SCHWARTZ, R.N., M.S.N., 
DOCTORAL STUDENT, DEPARTMENT OF EPIDEMIOLOGY 
AND PUBLIC HEALTH, SCHOOL OF MEDICINE, YALE 
UNIVERSITY, NEW HAVEN, CT 

Ms. Schwartz. Good morning, Mr. Chairman, and thank you very 
much. I want to thank you for these hearings. As I was sitting here 
this morning looking at what I am about to tell you, I was reminded 
of the sterility of statistics and how sanitized it can be. When you 
look at what it really means in human emotion, the importance of 
this hearing becomes quite clear. 

I am myself a woman veteran, retired from the United States Air 
Force. The information that I'm going to tell you about comes from 
the fact that I worked on the National Vietnam Veterans Readjust- 
ment Study, and when I was doing it, I realized that there were 
questions in there about physical health and reproductive outcomes 
of women who served during Vietnam. The beauty of this study was 
it was the first time that we'd be able to look at these health 
problems and compare women who served in Vietnam with military 
women who did not serve in Vietnam, and then there was another 
group to look at who were civilian women. 

So I'm going to talk to you first about when I looked at the women 
who served in Vietnam as compared to the others on their reproduc- 
tive outcomes. The women who served in Vietnam had statistically 
significantly more negative reproductive outcomes than did the 
Vietnam-era women or the civilian women, and by negative, I mean 
that they had more miscarriages, more stillbirths, and more children 
who died before the first year of age. They also had more diseases of 
the ovaries and the uterus, and they also had twice the rates of 
cancer of women who were civilians. 

Another thing that I found is that they had very high rates of 
multiple sclerosis. There were six cases of multiple sclerosis in the 
430 women in the study. 

Also, because the question begged an answer, and because the 
National Academy of Sciences was closing their books on the first 
part of their Agent Orange study and had not even considered the 
question of women, I was able to do this because this data in the 
study had the dates and the places that the women were stationed. 
What I did was take the schedule of the spraying missions that they 
conducted in Vietnam when they used Agent Orange, Agent White, 
and Agent Blue, and I created another variable to look at what 
happened to women who were right in those provinces of Vietnam 
when the spraying was going on, as opposed to women who were not 
in the provinces of Vietnam when the spraying was going on. 

I want to tell you that it was even worse. These women who were 
exposed or were in the provinces of Vietnam during the time of the 
spraying had more gjniecological diseases, including tumors of the 
ovaries and uterus. Forty-seven and a half percent of the women had 
negative reproductive outcomes, and 28 percent of these women 



34 

reported that 100 percent of their pregnancies ended in either a 
miscarriage, a stillbirth, or a child that died before the first year of 
age. 

I feel a real responsibility to also tell you that one of the things 
that impressed me about this data was the fact that these women 
who had so many miscarriages never stopped trying to have a child. 
Some of them had as many as 13. And when I met one of them, I 
asked her, "How could you do this? How could you keep on trying?" 
and her answer was, "Because I was surrounded by so much death in 
Vietnam, I wanted to try to be near life." 

I also want to share with you — I know you spoke about Judy 
Jacobs, but I want to tell you about the first time I ever met her. She 
called me at my home, and she said to me over the phone, "Have we 
any information on what happened to women and Agent Orange in 
Vietnam?" and I said, "No, we don't," and she said, "Well, I just 
wondered, because I've had 13 miscarriages. I've had a hydidoformal," 
which she called a baby. "I have three living children, and all of them 
have birth defects. I have cancer of the thyroid and stomach. I have 
non-Hodgkins lymphoma. I am diabetic. And I just wondered if this 
had anything to do with when I served in Vietnam." 

So I asked her where she served, and she told me, and I said, 
"What did they do there with Agent Orange?" She said, "We used it. 
We threw it out so we could keep the grass down. It was stored there. 
And then, when the barrels were empty, we cut them in half and 
used them for barbecue pits." 

I think you have heard a long trail of tears this morning, Mr. 
Chairman, starting with people not even recognizing, during World 
War II all the way up to the Persian Gulf, what they're dealing with. 
They can't even protect themselves, because they don't know what to 
protect themselves from. I hope there is some way that this Commit- 
tee will find to help those families that need the help now. 

Thank you for the opportunity to share my findings with you. 

[The prepared statement of Ms. Schwartz appears on page 254.] 

Chairman ROCKEFELLER. Thank you, Ms. Schwartz, and we will 
not fail. 

Mr. Chan. 

STATEMENT OF KWAI-CHEUNG CHAN, ISSUE AREA DIREC- 
TOR, PROGRAM EVALUATION AND METHODOLOGY 
DIVISION, U. S. GENERAL ACCOUNTING OFFICE 

Mr. Chan. Good afternoon, Mr. Chairman, and Senators Wellstone 
and Daschle. After what's happened before my testimony, I think my 
statement may appear a bit procedural and dry, but nevertheless I do 
understand that maybe in my testimony and our report, done at your 
request, somehow we'd like to bring these things together so that 
there's some way the Government can be more responsive. 

Chairman ROCKEFELLER. I think that's what people have been 
saying. They want research, they want understanding, and whether 
it's dry or not doesn't make any difference to them. They want the 
truth, and that's what you're going to tell us. 

Mr. Chan. Thank you for the opportunity to present our statement 
of potential reproductive dysfunction among U.S. Armed Forces who 



35 

served in the Persian Gulf, and that's the hmit that we have done. 
Today, at your request, we're issuing the report entitled "Operation 
Desert Storm: Questions Remain on Possible Exposures to Reproduc- 
tive Toxicants." 

Mr. Chairman, you asked us to address four questions. These are: 
DOD's assessment before the war, what toxicants did they identify, 
the education and protection afforded the troops during the war, and, 
finally, the monitoring efforts for reproductive dysfunctions after the 
war. 

We found that the health hazard assessment process that DOD 
used for assessing the potential for exposure to such toxicants before 
the war was incomplete. In its materiel acquisition process for 
equipment, DOD performed general health hazard assessments that 
may identify possible reproductive toxicants. It also relied on EPA's 
normal processes for screening pesticides. But no assessment was 
made on the effects from various individual and possible synergistic 
effects of compounds presented in the working environment of the 
deployed troops. 

Second, DOD generally endeavors to identify toxins and hazards 
that are internal to the weapons system development process. We 
identified 21 specific reproductive toxicants that were presented in 
the Gulf region, primarily in the oil well fires and also in pesticides. 

In terms of protection and education during the war about these 
toxicants, we found none directly applied; however, some of DOD's 
activities to protect against other hazards may have also minimized 
exposure to these toxicants. 

In terms of what they have done in monitoring after the war, we 
found a number of major shortcomings involving certain ongoing 
studies, the planned studies, as well as the VA and DOD registries. 

To conclude, then, 3 years after the war, basic questions remain 
concerning reproductive dysfunction among the veterans' community. 
The basis for this uncertainty is threefold: (1) certain potential 
reproductive toxicants were present, as we found; (2) for some 
toxicants, the exposures may have been widespread but were of 
unknown intensity; and, (3) the studies that have been performed to 
date are unfinished or are too weak methodologically to determine 
convincingly that there are or there are not abnormally high 
reproductive dysfunction rates among some Persian Gulf veterans 
and their families. 

In our report, we made four recommendations. First, the Secretary 
of VA should direct that VA use its revised and expanded question- 
naires to reregister the 20,000 or more veterans who had already had 
VA registry examination. 

Second, the Secretary of Defense, working in concert with EPA and 
HHS, should ensure that DOD makes additional scientific inquiry 
into the possible synergistic effects of multiple exposures to hazards 
found in the Persian Gulf. 

Third, the Secretary of Defense should explore approaches to 
collect baseline data on birth outcomes, infertility, and miscarriage 
rates among active duty and reserve personnel, so that these data 
are available for future studies. This information should include 
baseline data on exposure levels to ascertain when exposures of 



36 

reproductive toxicants rise to dangerous levels, particularly in future 
conflicts. 

Fourth, DOD should develop procedures to better ensure that 
troops are informed of possible reproductive toxicants before future 
deployments and to monitor exposure levels to such hazards. 

This ends my statement. Thank you. 

[The prepared statement of Mr. Chan appears on page 265.] 

Chairman ROCKEFELLER. Thank you, Mr. Chan. Your testimony is 
very brief. The study is more lengthy. 

Mr. Chan. Yes, sir. 

Chairman ROCKEFELLER. Let me start the questions, if I can, with 
Senator Daschle. 

Senator DASCHLE. Thank you, Mr. Chairman. 

I thank the members of the panel for yet another excellent series 
of presentations. I'm very grateful to each of you for the contribution 
you've made this morning. 

I would be interested, if we could, in using what limited time I 
have, to participate in a discussion of the recommendations made by 
the General Accounting Office and Mr. Chan. I would be interested 
in Dr. Paul's and Dr. Silbergeld's and Ms. Schwartz' response to the 
recommendations that GAO has made. Do you all have them before 
you? 

Dr. Paul, you don't have them before you? 

Dr. Paul. I don't. 

Senator DASCHLE. We can see that you all have copies in front of 
you. 

Dr. Paul. OK. Thank you. 

Senator DASCHLE. I think it is a plan of action that has merit, 
although it may be a conservative plan. I don't know that any of our 
witnesses have had the opportunity prior to this morning to consider 
the recommendations made by the General Accounting Office, but I 
would be interested in your reaction to them. 

Dr. Silbergeld? 

Dr. Silbergeld. I think that my concerns about the recommenda- 
tions relate to what they assume. They assume, I believe, that we 
know a great deal more than we do about how to conduct these kinds 
of recommendations. These are primarily surveillance and monitoring 
recommendations in one part. In another part, it is to bring together 
existing knowledge on potential reproductive developmental hazards 
that might occur both fi*om the Persian Gulf War and, as you've 
stated, to put us in a state of readiness in anticipation for anything 
in the future. 

I think that to truly implement these recommendations about 
going back and reregistering the veterans and applying more 
sensitive and comprehensive questions, which I believe is what your 
report states, Dr. Chan, and the third one, to collect baseline data on 
a number of outcomes, assumes that we have a good way of undertak- 
ing that kind of surveillance system. The data on birth outcomes, 
infertility, and miscarriage, in my opinion, represent the extremes of 
response. Those are very serious and significant outcomes, as we've 
heard today. 



37 

Fd suspect there is a whole range of dysfunctions and disabilities 
that are occurring in the range of people, based on their exposures, 
that would be extremely important to understand and collect 
information on, if only to serve as a warning signal and to help us 
understand better what goes on over the full spectrum of toxic effects. 

To collect existing information on the effects — ^the scientific inquiry 
on the possible synergistic effects of multiple exposures to hazards, 
there's nothing there. If you open that door, it's an empty room. You 
can direct DOD, you can direct HHS, you can direct EPA all you wish 
to get that information. It does not exist. And until you direct the 
agencies that can conduct and fund research to acquire that informa- 
tion, this is, I'm sorry to say, a meaningless recommendation. 

Senator DASCHLE. That's not encouraging, but it is certainly very 
helpful. 

Ms. Schwartz or Dr. Paul? First, I'd be interested in whether you 
share that observation, and, second, whether you would make other 
modifications or recommendations. 

Dr. Paul. I certainly share the observation about the synergism. 
We don't even know enough about just the baseline reproductive and 
developmental effects of many agents, never mind how they interact 
with each other, and I think that that information would be very, 
very hard to collect. 

I would just urge a couple of things: One, that we not think just 
epidemiologically, that, in fact, epidemiologic studies take forever, and 
at the end of them, there's often a tremendous amoimt of uncertainty. 
If we're going to design epidemiologic studies, that we do them 
incredibly well — in other words, not just to look at a population of 
veterans that were exposed in the Persian Gulf and just get frequen- 
cies of outcomes, but to design studies that look at cases and controls 
and compare outcomes, and that we think carefully about the types 
of epidemiologic studies that should be conducted to really have the 
best chance of giving us some good data. 

I think, especially in light of the kinds of complaints that we're 
hearing about that we've not heard about in the past, it's important 
for us — and perhaps we could do this through a registry — to learn 
more about what the actual case definitions are, how often they occur, 
what these conditions really look like. 

Then, I actually think it's important for scientists to begin to 
brainstorm about the biological plausibility that these effects might 
be due to certain agents. We must hypothesize a little bit, go to the 
animal data, and ask what do we know about these agents? What 
more do we need to know about these agents? How do they exert 
their effects? Is it likely that this pesticide might cause this kind of 
problem? And not just collect information on tons of exposures and 
tons of outcomes, without having first preliminary ways of thinking 
about what specific exposures might be most likely to be involved if 
there is in fact an association. 

Finally, as a clinician, I think I would like to reiterate the last one. 
I do really agree that we need to develop better procedures to be sure 
that troops are informed of possible reproductive toxicants before 
future deployments and to monitor exposure levels to such hazards. 
I'd add a couple of things. 



38 

I think it's important — and we see this in occupational medicine all 
the time — to think about having safer substitutes for toxic agents and 
not always to assimie that you have to use a toxic agent to accom- 
plish a purpose. And although it's probably not going to be possible 
for us to eliminate the hazards of wartime service, that we begin to 
think about these kind of things. What kind of substitutes can we use 
that will accomplish the same purpose without harming military 
personnel? 

The other thing I think is that it would be very important to 
establish a clearinghouse — and I'm not sure how to do this — for 
information. This could be very helpful, because we know there are 
physicians out there who are seeing people who are experiencing 
problems, and people may be getting ideas about what might be 
involved, about how to treat things. If we have a clearinghouse where 
we can begin to share that information and get it out to physicians, 
that's very important. 

I also, lastly, would say that from my clinical experience, it's 
extremely important that people be informed about what we know 
and what we don't know, and that it's fine that we don't know 
everything now. I realize from my experience with patients that it's 
OK to admit what we don't know, but if we don't tell people anything 
about what we do know, that's really a disservice. It's only through 
knowledge of potential hazards that people can take measures to 
protect themselves and not be using Agent Orange barrels as 
barbecue pits and being sure that when they handle something, that 
they wear appropriate protections £ind things like that. So hazard 
protection has to be an integral part of that information. 

Senator DASCHLE. Thank you. Dr. Paul. 

Ms. Schwartz? 

Ms. Schwartz. I spent 16 years in the United States Air Force, 
and military life is not a laboratory. I was willing to put my life on 
the line. One day I became injured, and I expected the Government 
to validate my service by taking care of me. What I think we've heard 
here this morning is that — I cannot believe, Mr. Chairman and Mr. 
Daschle, that somebody in America didn't know if you marched people 
through the center of the atomic bomb, something bad wasn't going 
to happen to them, and I don't believe that the people that sold us 
Agent Orange didn't know that something bad was going to happen, 
and they should have shared that with us. 

But the most important thing is the responsibility of our Nation to 
take care of these people when they fall prey to these unseen toxins, 
when their children are bom. It is a disgrace that I hear this morning 
that people who are serving in the military have to go to welfare and 
get another job to pay to take care of their children who are ill. That's 
a disgrace. 

Senator DASCHLE. Well, Ms. Schwartz, that leads me to my second 
question, and I'll try to be brief, Mr. Chairman. One of the reasons we 
have the policy we have has to do with what we're about to hear from 
CDC. CDC is saying almost exactly the same thing about the effects 
of exposure in the Gulf War that they were saying for many, many, 
many years on exposure to Agent Orange: There is no statistical 



39 

evidence or little statistical evidence that would indicate a dispropor- 
tionate effect on those who are exposed. 

Now, Ms. Schwartz, I heard you very clearly state what I consider 
the contrary. Your experience in Vietnam, your experience as a 
researcher seems to me to be very clearly in contrast to what CDC 
will tell us after this panel is excused. To what extent, in your view, 
is statistical evidence something that we ought to consider here? How 
do we weigh the CDC's analysis of what statistical effect there may 
be? Do we look at anecdotal information, as powerful as it has been 
this morning? Do we look at statistical information? How do we 
balance the two? 

We didn't do a very good job of it, in my view, in the Agent Orange 
controversy for many years, and finally, in exasperation, we said, 
"Look, we don't care. We're going to give the benefit of the doubt to 
the veteran." Unfortunately, many of them by then had died, had 
offspring that were sick, had an incredible array of problems that 
were still beginning to be fully realized. 

But here we are at the threshold of yet another situation similar 
in so many ways, with so many of the same circumstances confront- 
ing us again. We're confronted with the same questions. And so I ask 
you, how do we balance statistics and other very clear information 
that, in our view, is pretty compelling? 

Ms. Schwartz. I'll just respond to that. The National Vietnam 
Veterans Readjustment Study — and I'm sure you know a lot about 
it — was not a health study. I used all the variables that I could glean 
from it to help me understand if what I am telling you is in fact what 
it is, and I will stand by that. But I'm sure that there is — you know, 
statistics are one thing, and I'm sure the CDC is looking at it and 
saying to themselves, "Well, she's using data" — I mean, people can 
pick apart what I said just as clearly as they can do just about 
anything in this day and age. 

However, I think the point of view is that I bring this with the idea 
in mind that there has never been a study of the women who served 
in Vietnam. This Congress authorized it, funded it in 1986. The 
people have been arguing over "how are we ever going to do this 
study?" They say they can't find a cohort large enough. Why? Because 
each year we lose more of that cohort, Mr. Daschle. We bury them. So 
just like the generation of the World War II atomic survivors, they 
have gone by-the-by. 

The lessons that we learned fi-om the past, maybe you can't 
develop a foolproof way, but I believe that there are better measures 
that can be t^en to inform our troops or to develop things that will 
prevent this fi-om recurring at the rates we see today. But at the 
same time, I will bring you back to home base and say that when 
someone is injured in the line of duty, when someone suffers in the 
service of their country, it is the responsibility of this Nation to stand 
by them and to help them and not argue with them. It demeans their 
suffering, and we need to at least validate the pain that these 
families have suffered. 

Senator DASCHLE. Thank you. 

Dr. Silbergeld. 



40 

Dr. SiLBERGELD. I'd like somehow to transcend what I think is 
often an unfortunate battleground between the power of the kind of 
individual evidence and reports that we all hear and what seems to 
be the cold-hearted lens of statistics, which seems to make things go 
away. I guess as a professor in an epidemiology department, if I 
didn't try to do this, I'd lose my job. 

I'd like to suggest that there's actually an opportunity for a 
creative cycle here to get out of this constant battleground between 
the two camps of evidence, if you will. I believe very much — and I 
think Dr. Paul alluded to this — that what statisticians sometimes 
refer to disparagingly as anecdotes, clinicians call case reports, and 
the rest of us call personal experience provides very powerful signals 
of events, and that the integrity of those signals, of those reports 
should not be dismissed. 

Those signals should alert us to set in motion the finest and best 
techniques of rigorous examination. They should not be tested against 
them. They should be used as the starting point to develop case 
control studies, more sensitive indicators of both exposure and effect, 
and very critically, since most statistics are pretty simple-minded, a 
much better understanding of the background environment against 
which we're testing the critical hypotheses: Did the women in 
Vietnam, did the men and women in the Gulf War, did the veterans 
from the atomic bomb explosions and atomic tests, are they experienc- 
ing a greater burden of adverse outcomes and health impairments? 

We always test that against an implied background. The word 
"greater" implies greater than something else. We don't usually know 
what that is. So if we use these reports to stimulate us to design 
better studies, to use more sensitive methods to detect events, and to 
understand more critically and rigorously what we're looking for in 
the vast haystack of human experience, then I think anecdote, 
personal report, and statistics can work together. 

Senator DASCHLE. Well said. I thank the panel very much, and, 
Mr. Chairman, thank you for letting me go first. 

Chairman ROCKEFELLER. Thank you, Tom. 

I really agree with that. I think we are caught in that trap, and 
especially in Government, where sometimes people feel they can't 
afford to make a mistake. I think you can make a mistake in the 
university world, you can make a mistake and the world doesn't 
descend on you, but somehow in Government you're not meant to be 
able to make one. So as a result of that, because we don't want to, we 
make endless mistakes. 

And I think you're absolutely right that taking personal experience 
and rather than just saying because those are emotional and 
profound and deeply disturbing, that they shouldn't be used statisti- 
cally, that they're not valid statistically, that they're not a marker, as 
you say, for something more important, I think you're quite right, we 
should take our signals as early as we can get them from wherever 
we can get them and then go ahead and do the best possible science 
that we possibly can. 

Because the one thing we understand is that this is all going to 
proliferate. Even as we have nuclear proliferation, our toxic prolifera- 
tion in this world is now just unknowable. So it is, as John Glenn 



41 

said, the atom bomb of the future, and we have to start as quickly as 
we can £ind then get it into your hands and into the hands of 
scientists as quickly as we can. 

Mr. Chan. Mr. Chairman, can I make a comment about that? 

Chairman ROCKEFELLER. Please, yes. You have the right to 
respond, don't you? 

Mr. Chan. I think one of the problems I find is that there's a 
tendency to look for some special silver bullet to explain something, 
when in fact there might be a very broad set of toxicants that you 
find. So fi-om a statistical point of view, you determine what they are, 
but the problem we have in this study is that the first thing you 
searched for was weapons for chemical and biological warfare. This 
means looking for what the enemy has done to us, rather than what 
we have done to ourselves. 

So in searching for something that is outstanding to gain some 
insight usually when it's not present, then it's very difficult. You find 
a lot of little problems. I kept telling my staff, "With all these people 
with dizziness and losing their teeth and all these problems, how are 
they going to have children?" So, we don't even have that set of 
statistics. 

But what bothers me, in looking — you know, when I look at the 
statistics and what happened in this, I try to separate the factors: 
Something that's known before the war and something that's 
unknown before the war, something that is controllable during the 
war and something that's noncontrollable. I tried to separate them. 
And what we found are incidents as mentioned by people — you know, 
the misuse of the chemicals, particularly petroleum, and the use of 
diesel fuel for sand suppressions, when they're taking a shower, they 
found gas in the shower. Those are controllable events. They're not 
uncontrollable. They're known things that one should not do. And I 
understand people will say, well, war is hell, but one shouldn't do 
that, and that requires education. 

There are things we know but are noncontrollable. Such as using 
prophylactics for treatment before potential attack by chemical 
weapons. We had to do that, because the outcome would be much 
worse if you don't use it than to use it. So, therefore, it's known in 
terms of the short-term health effect, and we don't have any data on 
women, and I agree with that, but nevertheless we do that because 
not using it, it's worse. So, therefore, that's what I call imcontroUable. 

But there are also what I call the unknown, but they're controlla- 
ble, such as the smoke from oil fires. We didn't know it was going to 
happen, but once it happens, once you look at it and say, "What did 
they do during that period? Did people have masks on or didn't they?" 
Is it sufficient to inform the soldiers through the radio annoimcing? 
That's what they did. 

And there are things that, as stated in the recommendation, are 
imknowns which DOD and EPA need to look beyond. Because I would 
assume research should continue in petrochemicals, in dioxins and 
other things. You know, it's silly for GAO to recommend that they 
should continue those researches. But there are incidents, we 
understand, where pesticides may interact with the prophylactics 
that's not only additive, but there may be synergistic effects, which 



42 

is much worse. The accumulations of multiple chemicals that can 
affect an individual. And these effects are not what normally EPA 
would go and look for, because they're defined by that particular 
condition where the war is fought and what kind of things they put 
in there to allow soldiers to use and also potential abuse, not knowing 
what's the right thing because they weren't informed. 

So I think as you dissect them all, there are things that we can do, 
and there are things where we need more research. 

Chairman ROCKEFELLER. I've just learned. Senator Daschle, we 
have two votes that begin right now. Actually, that could be very good 
news, because there may be some people in here about to keel over 
from starvation as well as other things. 

So what I will do, so that we can go on to our third panel when we 
come back, is simply just say to each of you that I have about eight 
pages of questions aJl ready to go, but time has lapsed, and I can get 
those to you and you can get them back to me within a couple of 
weeks. So I think that will serve us well. 

National Geographic has come out with — I think it's the recent 
edition — a heartbreaking photograph, and it shows environmental 
toxins and what they've done to Russian children. You probably can't 
see these from here, but I'll leave these while Tom and I are going to 
vote. These are children missing part of their arms. But if you come 
and look at it, it's more than statistics here. So I'll just leave it right 
here at the front, and you can do that. 

This is incredibly important. The research that you are doing and 
what you're contributing, all of you, to this new body of knowledge is 
very, very important. I'm sorry that we have to cut this short, but 
Tom and I will get fired if we don't go vote, so we need to do that, and 
when I come back, we'll go on to our final panel. 

Thank you all very, very much, and we will send you the questions 
and appreciate your courtesy and patience. 

[Recess.] 

Chairman ROCKEFELLER. Our third panel consists of officials from 
the Department of Defense, the Department of Veterans Affairs, the 
Environmental Protection Agency, and the Centers for Disease 
Control and Prevention. 

Folks, don't sit down yet, because I'm going to swear you in. First, 
let me swear you in, and then I'll introduce you. Do you swear that 
in your testimony you will tell the truth, the whole truth, and nothing 
but the truth? 

[All witnesses respond in the affirmative.] 

Chairman ROCKEFELLER. Let the record show that all were 
affirmative. 

We have with us the Assistant Chief IVIedical Director for Environ- 
mental Medicine and Public Health at VA, Dr. Susan Mather, 
accompanied by Dr. Fran Murphy, Acting Director, Environmental 
Agents Service, VA; Dr. Sue Bailey, who is Deputy Assistant 
Secretary for Professional Affairs and Quality Assurance at the 
Department of Defense; George Siebert, who is Assistant Deputy 
Under Secretary for Safety and Occupational Health at DOD; Dr. 
WiUiam Farland, who is Director of the Office of Health and Environ- 
mental Assessment at EPA; and Dr. Henry Falk, who is Director of 



43 

the Division on Environmental Hazards and Health Effects at the 
Centers for Disease Control and Prevention, accompanied by Dr. 
Colleen Boyle, a section chief at the Division of Birth Defects and 
Developmental Disabilities at CDC. 

Now, my understanding is that CDC was going to offer testimony, 
but instead, you'll just include it in the record. 

Dr. Falk. I believe it has been included in the record. In view of 
the lateness of the hour, if you would like to proceed to the question- 
ing, that would be fine with me. 

Chairman ROCKEFELLER. OK. Everyone's prepared statement will 
be included in the record. 

[The prepared statement of Dr. Mather appears on page 270.] 

[The prepared statement of Dr. Falk appears on page 274.] 

Chairman ROCKEFELLER. Dr. Bailey, let me start with you. In their 
report, GAO concluded that DOD made virtually no efforts to warn 
Gulf War servicemembers that 21 pesticides and other widely used 
chemicals could harm their ability to have children. Do you have any 
explanation for that failure, if you agree with the allegation? 

Dr. Bailey. Well, I think when you look at the need for quick 
deployment and the kind of efforts that were made to inform military 
personnel about the risks, it falls into better context. I think, 
obviously, there are multiple hazards that people were exposed to in 
that situation, and it would have been impractical to go through all 
of the possible risks. 

I can tell you, as a reservist myself who was possibly deployable at 
that point, that we were taken into meetings and informed exten- 
sively about the kinds of hazards — parasitic hazards, water hazards, 
concerns about that particular area — but, again, I don't think it was 
really practical to go through every pesticide that might have been 
possibly hazardous, though it would have been wonderful to be able 
to do so. 

Chairman ROCKEFELLER. IMy impression, in trjdng to remember 
that war, was there was an enormously long buildup, and of all the 
wars certainly in my lifetime or that I can really think about, it was 
about the most systematically built up preparation for warfare, which 
then lasted for a relatively short period of time. There was about 4 
months of buildup. 

So when you say it wasn't practical, it seems to me that you would 
have had a sense what it was the Iraqis might have been throwing at 
us. You knew what that was pretty well. You knew what it was that 
you were going to be using to try and counter that to protect our 
troops from that. 

Dr. Bailey. Absolutely. I would suggest that is why, for instance, 
there were some of those particular immunizations given that now 
are in question, because indeed they may have caused some problems. 
But at the same time, we knew we might encounter anthrax, 
botulism, and so, indeed, we gave immunizations for those particular 
things, as you say, that were going to be thrown at us. 

Let me also remind you — 

Chairman ROCKEFELLER. But that's not true on botulism. I mean, 
I think on botulism, in most cases, the series of vaccinations weren't 
completed. 



44 

Dr. Bailey. Well, what I'm saying is there were things that we 
knew — for instance, with p3rridostigmine — that we were concerned 
that there would be chemical and biologic warfare, so there were 
things that were given specifically to deal with those that we might 
encounter. 

Let me also remind you, Mr. Chairman, that there was an 
extensive usage of Guard troops and reservists, so that those among, 
for instance, my unit, 2306 at Bethesda Naval Hospital, they were not 
there all the time. These are people that drill once a month. So some 
of the preparation was not the type that you would use with active 
duty personnel. 

Chairman ROCKEFELLER. I'll try my best to understand that. Why 
would you differentiate between active duty personnel and reservists 
if all had the possibility of being in the theater? 

Dr. Bailey. Well, I'm just responding to the fact that you're 
indicating we had an extensive buildup time to prepare, and I'm just 
suggesting — 

Chairman ROCKEFELLER. Isn't that relatively true, relative to 
most? I mean, it wasn't exactly Pearl Harbor. 

Dr. Bailey. Well, what I would suggest is, when you have people 
who are drilling once a month, for instance, that it may be more 
difficult to do so. That does not mean that I do not think it is a good 
idea to inform people to the utmost of our ability of any potential 
hazards, and that is something we consider — we are at this point 
taking into consideration as we prepare for deployments in the future. 
Serious consideration, so that people are informed. 

Chairman ROCKEFELLER. The whole question of toxins, and the 
reproductive consequences of some of the medical products you were 
issuing and having soldiers take, was not, I take it, discussed. Did 
you know about the possible effects, for example, in some of the 
testimony that was given this morning? Did the military know that 
that might be a possibility? 

Dr. Bailey. Well, I think, for instance, as far as pesticides go, it's 
interesting that the pesticides that were used were of less damaging 
possibilities than the ones that are used currently here in America in 
agriculture, the point being that they were trjdng to use the safest 
possible methods to give the best possible protection to the units that 
were going to be deployed. 

Chairman ROCKEFELLER. But you will admit it was insufficient. 

Dr. Bailey. Well, there were also preventative medicine — 

Chairman ROCKEFELLER. Just for my sense of balance. 

Dr. Bailey. Well, I would also remind you that preventative 
medicine personnel were deployed with those troops to the Gulf, and 
preventative medicine was something that was considered and 
continues to be considered. Can you always list every particular 
pesticide when you're looking at time trying to protect your troops 
from potential hazards? That would be the ideal. I'm not sure that 
that's always practical. 

Chairman ROCKEFELLER. But shouldn't your answer be, almost 
regardless of the facts, I mean, just from the point of view of dealing 
with Congress or dealing with people in this country, that, yes, you 
should have tried to warn them of 21, or whatever it was, different 



45 

toxins that were available, that you should have tried to do that, but 
in fact that you were not able to, and that you regret that you 
weren't, and that you're planning to never have that happen again, 
rather than saying, "It wasn't practical to do it, so we didn't do it," 
and you never can anticipate what's going to happen in war, and, 
therefore, you don't try to anticipate? 

Dr. Bailey. You're absolutely right. I think that we should always 
be trying to warn our troops of potential hazards, and I think we 
intend to do so in the future. After listening to the testimony today, 
for instance, as I consider what happened with Agent Orange, I am 
pleased to say that there are steps that have been taken, such as this 
hazardous chemical warning label, which would have been on those 
Agent Orange cans, so that they would not have been used as a 
barbecue, for instance, and in fact people would have been very 
careful with the substance. So I do think that we try to learn from 
every deployment and make the appropriate changes in our behav- 
iors. 

I would also want to add that we have here — this is for Somalia. 
Operation Support Hope. This is given as a risk management leaders 
guide, and it does go through extensively the kinds of things you're 
talking about. So we are making the changes that you suggest and we 
rightfully should do. 

Chairman ROCKEFELLER. And if that had applied to the Persian 
Gulf, how would that have been used? In other words, you hand 
somebody a pamphlet — is that written in language that most people 
would be able to understand? Is it a list of scientific chemicals? 

Dr. Bailey. It is a leaders guide, yes, and it would have the 
chemicals and risk management issues related in ways that could be 
understood. 

Chairman ROCKEFELLER. Could I get a copy? 

Dr. Bailey. You absolutely can. 

Chairman ROCKEFELLER. Right now? 

Dr. Bailey. This one is incomplete, is it not? 

Mr. SlEBERT. We can submit it for the record, sir. 

Dr. Bailey. We're going to submit it for the record. These are not 
as complete as what would be issued. 

[The referenced guide was subsequently provided and is contained 
in Committee files.] 

Chairman ROCKEFELLER. Thank you. So in other words, you — 

Dr. Bailey. To let you know what's in them, there are things — 

Chairman ROCKEFELLER. No, no, I'm going beyond that now. I'll 
see what's in them, because I'm about to get it. But the concept that 
21 reproductive hazards were out there, that there is a whole new 
concept — in my life, at least — called "shooting fire," which is just 
almost like movies that haven't been created yet, the thought of it is 
so devastating, the implications of it are so devastating. I'm not 
prepared to say and don't know how that happened and why it 
happened, but it would just seem to me that the miUtary, when they 
testify — I assume you heard the testimony this morning? 

Dr. Bailey. Yes, sir, I did. 

Chairman ROCKEFELLER. I would think that your attitude should 
be that we're never going to allow this to happen again. I mean, just 



46 

in terms of your own integrity, of your own agency which you 
represent — 

Dr. Bailey. Absolutely. 

Chairman ROCKEFELLER. As opposed to saying it's not practical to 
do. I mean, that's what your testimony was. See, this is what causes 
suspicion on the part of people like myself. "It wasn't practical." Then 
you amended your testimony as I put pressure on you to do that, but 
your testimony was it wouldn't have been practical to do that. That's 
one of the reasons people don't really love Government a whole lot, 
because that's not what they want to hear from Grovernment when 
they see the results of what it is that Government did or Government 
caused to happen because Government sent these folks into battle. 

You say this is Operation Support Hope. Is this for Rwanda? 

Dr. Bailey. One is for Rwanda, and one is for Somalia. 

Chairman ROCKEFELLER. OK. And so my question is, what kinds 
of preparations are you doing for those theaters? You have this, which 
I will look at — 

Dr. Bailey. For example, here's a memo. "This is to request Joint 
Chiefs of Staff assistance to ensure that all personnel employed to 
remote locations are apprised of potential environmental health 
hazards and are instructed in methods to protect themselves from 
occupational and environmental illnesses inherent in the area of 
operations. 

"U.S. forces deployed to Rwanda face a significant threat from 
communicable disease and vector-borne disease. In addition, there 
may be environmental health threats posed by pesticides, herbicides, 
fuels, and other hazardous materials/equipment associated with the 
relief operation. 

"It is essential that DOD take aggressive action now to identify 
potential hazards, collect exposure information, including the use of 
pesticides, document personnel protective measures implemented, and 
identify and reward DOD personnel or units serving now or in the 
future in Rwanda. Proactive efforts will help protect the health of 
deployed personnel and be extremely useful for possible medical 
followup. 

"The militatry departments have the public health and environmen- 
tal expertise to recommend effective preventative measures. Country- 
specific disease threat analyses are also available from the Armed 
Forces Medical Intelligence Center and the Armed Forces Manage- 
ment Board. Predeployment briefings based upon good medical 
intelligence will answer questions about possible adverse health 
effects and communicate true risks to our personnel and their family. 

"These data, supplemented by on-site hazard analysis, are 
necessary to program meaningful health precautions and to evaluate 
the potential long-term health risk to our personnel." 

Chairman ROCKEFELLER. OK. Let me stop you there. It's what I 
would call "government language." It's not the kind of thing that folks 
from my State would pick up and say, "I think I'll plow right into 
this. It sounds really exciting." What you gave to me was one 
paragraph and then a table of contents, and on the table of contents, 
it indicated that the last chapter, which is chapter 7, starts on page 
73. 



47 

Dr. Bailey. There's a packet- 
Chairman Rockefeller. So I assume it's a rather large book. So 
my question to you, then, if it's something Uke this, you pass it out, 
how do you make sure people read it? 

Dr. Bailey. Well, I think to go back to my question about 21 
pesticides, as a physician, if I tell you a drug may have some possible 
side effects, I don't read you the entire page from the PDR. That's 
what's impractical. I'm not saying warning people about real threats 
to their own health is impractical. I do not mean that at all. I mean 
that to inform them, "These are a list perhaps of pesticides, these are 
problems that may be associated" — 

But, as you say, I don't think the Government language in the kind 
of detail that may really be available to us necessarily is appropriate 
for dispensing to every particular member of the military personnel. 
They should have information that's appropriate, and that should 
include that pesticides, just as I've described, are going to be in the 
arena and that those can be harmful and what they can do to protect 
themselves from that exposure. 

Chairman ROCKEFELLER. Sometimes, knowing the nature of human 
beings, they get thin books like this, much less fatter books like this, 
and they tend not to read them, which leads me to the conclusion 
that often you can do things better through oral communication. You 
get the troops under a tent or in a barrack or in some hall, and you 
lay down the law, "Look, this is what we're up against, we're not 
kidding, you better watch out, these are the things, you've been given 
this rather large volume," and then down through your command 
structure, you make sure that somehow people are at the meetings, 
hearing the oral warnings, are thus motivated, perhaps using 
examples from the Persian Gulf War, that this is something they 
really ought to follow up. I mean, you understand what I'm trying to 
say. 

Dr. Bailey. Absolutely. 

Chairman ROCKEFELLER. How you really get it into the minds and 
instincts of men and women? 

Dr. Bailey. Well, and that's why these are really for the leaders. 
There are briefings to be done from those books to the troops. 

Chairman ROCKEFELLER. And the briefings are done? 

Dr. Bailey. And the briefings are done. 

Chairman ROCKEFELLER. And, those are in what form? You 
indicated that you yourself had some. 

Dr. Bailey. Absolutely. Medical briefings, briefings about the 
arena, what we would be encountering, what to put in your sea bag, 
things like that. So that, as you say, it is put into a form that people 
are able to use. 

ChEiirman ROCKEFELLER. Yes. And also there is some sense that we 
could have done a bit better in the Persian Gulf. 

Dr. Bailey. I think we can always do better, and I think we've 
learned — 

Chairman ROCKEFELLER. Now, don't tell me we can always do 
better. If you believe it, tell me yes, and if you disagree, then disagree 
with me and have an honest disagreement. But you could have done 
better in terms of warning our men and women who were going over 



48 

there to fight. Whether they were reservists or not, we could have 
done better in warning them. 

Dr. Bailey. Yes. 

Chairman ROCKEFELLER. That's fair. This is to you, Dr. Bailey, and 
to Dr. Mather. This morning we heard some very compelling 
testimony about the sexual problems that Gulf War servicemen and 
their wives are having. These problems seem to be related to 
something in the veterans' semen, which may even be causing birth 
defects and which appear to be doing that. 

According to scientists, the semen should be tested for pesticides, 
heavy metals, or other abnormalities, and yet Kelli Albuck told us 
that the mihtary hospitals refuse to do the necessary tests to find out 
what is wrong. Is there a reason for that, and what assurance can 
you offer to this Committee that DOD and the Department of 
Veterans Affairs will do this testing in the very near future? 

Dr. Mather. I think one of the first things we need to do in VA is 
to get together a group of urologists and reproductive specialists who 
can provide us with guidance on exactly what we should be testing. 
Certainly, the referral centers have the capability of doing this kind 
of testing when we understand what it is we need to be looking at. 

I'm accompanied by Dr. Murphy, who, until recently, was the 
director of the referral center in Washington, DC, and has personally 
examined a great number of Persian Gulf veterans, and I do want to 
assure you. Senator Rockefeller, that neither Dr. Murphy nor I 
consider these stories to be anecdotal evidence. We consider them to 
be very important clinical histories that we in the VA and our 
clinicians need to be hearing, so we thank you for that. 

Chairman ROCKEFELLER. You thank me for that? 

Dr. Mather. Well, you were the one that held this hearing, and so 
we — 

Chairman ROCKEFELLER. But that's the problem. I mean, that's 
precisely the problem. Hearings shouldn't be necessary to bring these 
things to your attention. 

Dr. Mather. And we have invited the veterans to come to VA for 
registry examinations and, if appropriate, for referral to the referral 
centers. 

Chairman ROCKEFELLER. You mean the veterans that testified this 
morning? 

Dr. Mather. Yes, and I believe Dr. Murphy spoke to Mr. Albuck. 

Dr. Murphy. I've had the opportunity to speak to both Troy and 
Kelli about their problems, and Troy was one of the early participants 
in the VA registry examination. He also had gone down to the 
Houston referral center, and we've offered him the opportunity, in 
addition, to come back for a reevaluation in Washington, DC. 

Chairman ROCKEFELLER. And beyond him? Beyond them, rather. 

Dr. Mather. We invite all Persian Gulf veterans to come in for a 
registry examination — 

Chairman ROCKEFELLER. And how do you do that? 

Dr. Mather. We have outreached through the media, through the 
veterans service organizations, we are outreaching through the family 
support program, which is an extremely important part of the VA's 
Persian Gulf approach, the family support program, which is an 



49 

outreach program into the community and a support program for the 
famiUes. 

Chairman ROCKEFELLER. And is it being more successful than it 
was with me, since I didn't know about this until I prepaired for this 
hearing? I mean, are you getting responses? 

Dr. Mather. Well, we've certainly testified to the effect that we 
had a registry program — 

Chairman ROCKEFELLER. Well, I understand that, but in terms of— 

Dr. Mather. — before this Committee in the past, I think. But we 
do welcome the press coverage, because you can reach with one 
television show so many more people than the veterans service 
organizations or outreach counselors can. So, I think that's an 
important function. I know that's not your primary function, but for 
us, it's an important function. When USA Today carries a front-page 
story that says veterans should come in for registry examinations as 
a part of the — 

Chairman ROCKEFELLER. So why was it that we had to give that 
interview, so to speak, as opposed to you? 

Dr. Mather. I don't think you did have to, but it's a help when you 
do. 

Chairman ROCKEFELLER. But my point is it should have — 

Dr. Mather. We've been saying this, too. We just don't have the 
audience that you have. Susan Mather doesn't make nearly as big a 
splash as Senator Rockefeller does. 

Chairman ROCKEFELLER. Well, that sounds nice, but you could 
make a lot bigger splash. I mean, this goes back to the whole question 
of sort of the predisposition of an individual or of an organization. I 
mean, I have — 

Dr. Mather. We would like all 600,000 to come. 

Chairman ROCKEFELLER. Could I finish, please? I have had this 
ongoing discussion, shall we say, with the Secretary, about do we 
treat Persian Gulf War syndrome illnesses or do we not, and I keep 
getting the answer back that the law says that we can't, and we can't 
do it until the Congress says that we tell them to, and I'm quite 
certain and, more importantly, other lawyers are quite certain that 
you can. 

So when I look at the VA, I look at you in terms of resisting — a 
predisposition to resist doing this kind of thing. So it's not just the 
soldiers that you have to convince — convincing me will be hard 
enough, but convincing them or getting to them, I think, is what 
counts. 

Dr. Mather. Yes. I'm really sorry. This is one of Secretary Brown's 
top issues, and he's been speaking about this around the country. 

Chairman ROCKEFELLER. Well, then, tell me how your outreach 
works, so that the folks who are here before us this morning — 

Dr. Murphy. I think we have a number of outreach efforts which 
have been very effective. We have had social workers and our health 
care providers go out and speak to Reserve units and National Guard 
units, telling them about the registry program, inviting them to come 
in for the registry examination. 

In addition, some of the Central Office staff have also been active 
in outreach efforts. For instance, on September 24 and 25, we have 



50 

an outreach effort which we've planned in the Midwest. We're 
spending a weekend going to four VAMC's, speaking to veterans and 
their famihes about the special issues of Persian Gulf health and 
telling them about the programs that VA designed especially for 
them. 

We have several special efforts, including the registry program and 
the referral centers for patients with unexplained illnesses. VA has 
the Baltimore Depleted Uranium (DU) Center to study the special 
problems of those veterans wounded by DU in the Gulf War, and the 
Birmingham Pilot Program, which is looking at the possible neuro- 
cognitive effects of chemical warfare exposure, if that occurred. 

So I think the VA has been active in designing appropriate 
programs for these veterans. We certainly know that our communica- 
tions have not always been as effective as we would like, but we are 
making great efforts in improving them. 

Chairman ROCKEFELLER. OK. Dr. Bailey, do you have an answer 
to the same question? 

Dr. Bailey. I do. If I could also go back just for a moment, because 
I think it was a very good question, because it came up today in the 
testimony earlier about the GYN effects, and I did want to mention 
that the DOD has one of the few OB/GYN occupational medical 
specialists and has recently established a reproductive hazards review 
board made up of civilian and military experts in the field of 
reproductive toxicology, occupational medicine, obstetrics and 
gynecology, industrial hygiene, and preventative medicine. So that 
clearly will be something that I have heard today that I would like us 
to look into extensively. 

As far as our outreach attempts, we have had press briefings, we've 
certainly put the word out through the Military Times, we have a 1- 
800 number, and currently there are thousands involved in the 
comprehensive clinical evaluation program through the DOD. We 
have numbers within Phase I, and, again, a total of thousands of 
people that are currently going through the program. 

Might I also add that that the CCEP, or comprehensive clinical 
evaluation program, is one of the most extensive medical evaluation 
programs that I think clearly I've seen in my medical experience. 

Chairman ROCKEFELLER. My life today is cursed by votes. There's 
one that's ongoing now, and there are 8 minutes left, and it's going to 
be 3 p.m. in the afternoon before I get back. I have 12 additional 
questions for you. Dr. Bailey; about eight for you. Dr. Mather; some 
for you. Dr. Murphy; and. Dr. Falk, I have four for you, and I have 
five or six for EPA. 

What has happened at this point is that canying this hearing out 
to its completion is not possible. So I'm going to write personal letters 
to each of you, and the questions will be in the form of personal 
letters to each of you, which will be signed by me, and I'd like to get 
those letters back with some fulsome answers on what I consider a 
rather fulsome subject. 

I'm extremely apologetic to you, but we started at 10:30, and it's 
going to be 3:15 before I get back, and I can't go on. I can ask you 
questions through the mail, I can get answers through the mail, and 



51 

I can, through Diana Zuckerman, Jim Gottlieb, and Patty Olson, 
follow up on the answers that I get from you. 

So on that rather discouraging note, I will have to say I'm sorry 
that we didn't get a chance to do this more thoroughly. One of the 
things we have to do here is vote. But we will do it thoroughly, and 
we'll do it through another form of communication, which will work 
perhaps just as well. 

Do you want to say something. Dr. Falk? 

Dr. Falk. Yes. I believe Senator Daschle had raised a concern 
which we would be happy to address in a similar manner. He had 
spoken about a dichotomy between statistics and — 

Chairman ROCKEFELLER. Yes, he had. 

Dr. Falk. I would like to address that and so would be happy if 
you would like us to address that. 

Chairman ROCKEFELLER. That's fine. You had to wait around all 
day, and you didn't get to say anything, and I totally apologize to you, 
but that's the way it has to be. 

This hearing is adjourned. 

[Whereupon, at 2:40 p.m., the Committee adjourned, to reconvene 
at the call of the Chair.] 



APPENDIX 1.— PREPARED STATEMENTS OF 
COMMITTEE MEMBERS 



PREPARED STATEMENT OF CHAIRMAN JOHN D. 
ROCKEFELLER iV 

From the earliest days of our Nation's history, our government has 
expressed its commitment to help veterans who were wounded in battle. But, 
unseen hazards, which are unrelated to the battlefield, can also create 
devastating medical problems. Those unseen hazards may not become obvious 
until long after these men and women have left military service. 

As the nature of military service changes, we must rethink veterans' medical 
needs. Just consider the humanitarian military activities in Rwanda this week, 
or the Persian Gulf War, where months of waiting in the desert and a few days 
of ground war may have created more medical problems from toxic exposures 
than from battle wounds. Yet these veterans were truly injured. 

Today, when we try to meet the health needs of veterans, we need to 
continue to consider physical and mental battle wounds and the scars they leave 
behind, but we also need to think about the more subtle and sometimes long- 
term risks of unseen enemies such as diseases and chemical exposures. 

Today we will focus on how these unseen enemies may eventually prevent 
veterans from having children or may increase the likelihood of birth defects 
or cancers among their future offspring. 

Of course, when our men and women are sent to war, their future fertility 
and the potential for birth defects are not their main concerns. And, for many 
reasons, neither the Pentagon nor VA has worried about those risks, made 
efforts to reduce those risks, or spent money to study those risks. 

Nevertheless, many veterans are experiencing serious reproductive problems, 
and they wonder if these problems were caused by their military service. The 
first major complaints came from atomic veterans and Vietnam veterans 
exposed to Agent Orange; both groups of veterans believed that military 
exposures had caused infertility or birth defects. In recent months, similar 
concerns have been repeatedly expressed by Persian Gulf veterans. All these 
men and women went to war, willing to face great danger or even death — but 
they never expected their future children to suffer. 

The purpose of today's hearing is to listen to those concerns. We will hear 
from veterans and their wives and widows, and from scientists from across the 
country, including some in the Administration. We will also be asking 

53 



54 

questions about what the Pentagon and VA have done in the past to address 
these questions. I hope that we will also hear how they expect to do better in 
the future. 



Statement of Senator Thomas Daschle 

Hearing of the Veterans Affairs Committee on Reproductive Hazards 

and Military Service 

August 5, 1994 

It is well known that military service carries with it the risk of possible physical and/or 
psychological harm. This is a risk that countless numbers of American men and women have 
accepted as a part of their service to their country. But it is important to remember that this risk 
goes hand in hand with our nation's obligation to care for these men and women if they do become 
harmed as a result of their military service. 

In earlier times, it was easy to say that a physical injury was caused by an individual's military 
service. That's because the injury was apparent - a broken bone, a gunshot wound. But in the 
20th century, the relationship between military service and adverse health effects has become 
increasingly complex. For example, we now know that soldiers exposed to a variety of hazards 
during service have developed diseases such as cancer and leukemia. Showing a connection 
between these diseases and military service, however, is usually quite difficult. 

And so it is with'the possible connection between military service and adverse effects to 
reproductive health. Given the variety of hazards to which our soldiers have been exposed - 
Agent Orange, ionizing radiation and other toxins -- 1 think it likely that these hazards have played 
a part in the stillbirths and neonatal deaths, birth defects, spontaneous abortion and infertiUty 
experienced by these soldiers and their offspring. Demonstrating this connection scientifically is 
another story. 

Today we will hear from members of the scientific community who can tell us what is known 
about the possible reproductive hazards associated with military service during World War II, the 
Viemam War and the Persian Gulf War. Perhaps more importantly, these scientists will be able to 
tell us what further research is needed to determine whether there is indeed a link between these 
exposures and adverse effects to reproductive health. 

Throughout my career in Congress, I have worked extensively on behalf of veterans exposed to 
Agent Orange during their service in Vietnam. Because this committee has never before 
investigated the possible connection between military exposures and reproductive problems, I 
would like to touch briefly on an issue that has received little attention over the years -- the Air 
Force's research concerning Agent Orange and reproductive effects that was undertaken as part of 
the Ranch Hand study. This ongoing study attempts to examine the health effects of Agent Orange 
exposure by examining those who were involved in Operation Ranch Hand, the aerial spraying of 
herbicides to defoliate the jungles of Vietnam. 

In January 1984, the Air Force issued its baseline morbidity report on the Ranch Hand study. 
Because an increase in birth defects, learning disabilities and neonatal deaths had been detected, a 
follow-up report was promised. By December, a draft of the "Reproductive Outcomes Update" 
was completed. 

This draft report indicated a doubling of the risk of having children with birth defects in the Ranch 



55 



Hand group. Despite this significant finding, the White House Agent Orange Working Group 
recommended that the report not be pubhshed. And despite my repeated efforts to obtain a copy of 
this draft report from the Air Force, it was not released until 1990, six years after it was written. 
As of last November, a final report had still not been published. 

There is a great deal more to this story, and the information that I am submitting for the hearing 
record tells that story. I would simply note here that I believe the Air Force should have publicized 
its preliminary findings and let veterans know about the potential harm to their reproductive health. 
I also believe if the Air Force had promptly followed up on this data and verified the findings of the 
1984 draft report, we might have a better understanding today of the association batween dioxin 
exposure and reproductive health. 

In its July 1993 report on the available scientific literature on exposure to herbicides, the National 
Academy of Sciences concluded that "the available studies are of insufficient quality, consistency, 
or statistical power to permit a conclusion regarding the presence or absence of an association" 
between exposure to herbicides and the following health effects: spontaneous abortion, birth 
defects, neonatal/infant deaths and stillbirths, low birthweight, childhood cancer in offspring and 
abnormal sperm parameters and infertility. In hght of this conclusion, NAS recommended that 
"priority be given to additional research on reproductive effects that would help clarify the possible 
effects of herbicides. In particular, the committee believes that extensive reanalysis of the Ranch 
Hand reproductive data could shed additional light on these questions " (emphasis added). 

I believe this NAS recommendation is an important one, and I intend to work with my colleagues 
on this committee to ensure that this data is reanalyzed in accordance with the NAS 
recommendations. I also feel strongly that the Ranch Hand data should be made available to 
independent researchers in order to advance our knowledge about the effects of dioxin exposure. 

I applaud Senator Rockefeller and his staff for calling this hearing and beginning - for the first 
time '- a frank and honest discussion about the reproductive health hazards of military service. 



56 



/^^pifYy^^^ 



CHRONOLOGY: AGENT ORANGE AND BIRTH DEFECTS 
AIR FORCE "RANCH HAND" STUDY 



January 1984 



December 1984 



November 1985 



Air Force release of "Baseline Morbidity Report" on the Ranch 
Hand study 

- detects increase in birth defects, learning disabilities and neo-natal 

deaths 

- promises specialized follow-up report ("Reproductive 

Outcomes Update") 

- Air Force assessment of findings: results are "reassuring" 

( 1 ) increase pertains to minor birth defects 

(2) increase might easily be explained by an 

overreporting of birth defects by Ranch Hand 
parents 

Draft of Reproductive Outcomes Update is completed but not released 
Findings: 

** doubling of risk of having children with birth 
defects following service in Vietnam 

- increase is for ALL defects, not just minor ones 

- increase NOT due to overreporting by Ranch Hand parents 

Article in San Antonio Express quoting Colonel William Wolfe, the senior 
investigator of the Ranch Hand study, as suggesting that the Air Force's 
conclusions from early 1984 were still valid (i.e., detected birth defects are 
minor and increase in birth defects among Ranch Hand children is due to 
overreporting) 



July 1987 Letter from Senator Thomas Daschle to Air Force requesting copy of 

December 1984 draft of Reproductive Outcomes Update 

August 1987 Letter to Senator Daschle from Colonel Wolfe, Dr. Joel Michalek 

and Dr. Richard Albanese confirming that a draft of the Reproductive 
Outcomes Update did exist and "was submitted to the Advisory Committee 
[a subsidiary of the White House Agent Orange Working Group] but they 
reconmiended that it not be published." 

- letter explains that since completion of 1984 draft, bias from overreporting 

of birth defects has been ruled out but "potential bias from 
underreporting remains" 

- letter predicts that data collection for the study would be completed by 

November 1988 and a final report would be issued soon thereafter 

- letter does NOT address Senator Daschle's request for a copy of the 

December 1984 draft report 

November 1987 Letter from Colonel Wolfe in response to inquiry from Daschle staff for 

copy of 1984 draft report 

- Wolfe is "unable to locate a copy of the draft" 

- letter also indicates that "an analysis of the partially verified birth defect 

data" was carried out in late 1984 



57 



December 1987 



January 1988 



February 1988 



May 1988 



June 1990 



1992 



July 1993 



followup letter from Senator Daschle to Air Force, again requesting that the 
1984 draft be released 

- letter also requests release of the 1984 analysis of the partially verified 

birth defect data alluded to in Colonel Wolfe's November letter 

meeting between Air Force officials, Air Force scientists (Colonel Wolfe, 
Dr. Michalek and Dr. Albanese) and Senator Daschle to discuss the status of 
the Ranch Hand study 

- Air Force refuses to release the 1984 draft of the Reproductive Outcomes 

Update 

- scientists verify that the 1984 draft report showed an approximate 

doubling of Ranch Handers' risk of fathering children with birth 
defects 

- scientists confirm that the defects were not necessarily minor and that 

the increase in defects was not due to overreporting by Ranch Hand 
parents 

- Senator Daschle requests that the Air Force issue a report clarifying the 

incorrect information on birth defects contained in the 1984 Baseline 
Morbidity Report 

- such a report had been drafted by Wolfe. Michalek and Albanese in 1985 

but had not been cleared by the Air Force 

- Senator Daschle to Air Force: release the 1985 report within a reasonable 

time or I will release this information to the public; Air Force agreed 

Air Force releases clarifying report with the names of Colonel Wolfe and 
Dr. Michalek removed 
Fmdings: 

- analysis of the applicable data "reveals a statistically 

significant increase in reported birth defects in the 
Ranch Hand group" 

- while dioxin cannot be "confidently identified as the 

causative agent," it can't be ruled out either 

- at a hearing of the Senate Veterans Affairs Committee, the Air Force seeks 

to discredit this report and de-emphasize its importance 

- under questioning, however, Air Force officials admit that the report 

is technically correct and that all three scientists (Wolfe, Michalek 
and Albanese) wrote it 

Air Force releases 1984 draft of Reproductive Outcomes Uptdate to 
Representative Ted Weiss, Chairman of the House Government Operations 
Subcommittee on Human Resources and Intergovernmental Relations) 

Air Force releases updated analysis of Ranch Hand baseline data 

- although a higher level of birth defects was found in the Ranch 
Hand group as opfxjsed to the control group, the authors of the 
study concluded that there is "no underlying association" in the data 
between birth defects and dioxin exposure 

National Academy of Sciences issues "Veterans and Agent Orange: Health 
Effects of Herbicides Used in Vietnam," a review and evaluation of the 



58 



available scientific and medical evidence regarding herbicide exposure and 
resulting health effects 

- NAS determines that "the available studies are of insufficient 

quality, consistency, or statistical power to permit a 
conclusion regarding the presence or absence of an 
association" between exposure to herbicides and the 
following health effects: spontaneous abortion, birth defecu, 
neonatal/infant deaths and stillbirths, low birthweight, 
childhood cancer in offspring and abnormal sperm 
parameters and infertility 

- with respect to the 1992 Air Force report, the NAS comments: 

"[T]he total prevalence of birth defects in the Ranch Hand 
group is greater than that in the unexposed comparison 

group These results are only suggestive but do indicate 

some difference in the risk of birth defects between these 
two groups. Based on their analyses incorporating serum 
dioxin levels, the investigators concluded that dioxin levels 
do not explain the difference. However, the committee is 
concerned about the methods and presentation employed in 
the analysis of dioxin levels, and it is unclear what the 
findings from this important study mean ..." 

- NAS concludes that "[s]ome aspect of the Ranch Hand experience 

seems to have increased the risk of fathering children with 
birth defects, but the implications of this finding are 
unclear." 

- the NAS report reconunends that "priority be given to additional 

research on reproductive effects that would help clarify the 
possible effects of herbicides. In particular, the conmiittee 
believes that extensive reanalysis of the Ranch Hand 
reproductive data could shed additional light on these 
questions." 

November 1993 Senate Veterans Affairs Committee ~ Staff Forum on Future Research on 

Agent Orange • 

- Dr. Richard Albanese indicates that the Air Force has not yet 
published a final version of the 1984 Reproductive Outcomes 
Update and that this report was not included in the National 
Academy of Sciences' review of the scientific literature on exposure 
to herbicides 



/"^ffm/^^^a^chi 



PROJECT RANCH HAND II 

AN EPIDEMIOLOGIC INVESTIGATION OF HEALTH 

EFFECTS IN AIR FORCE PERSONNEL FOLLOWING 

EXPOSURE TO HERBICIDES 

REPRODUCnVE OUTCOME UPDATE 
17 DEC 84 




Prepared for: 
The Surgeon Genera! 
United States Air Force 
Washington. D.C..20314 



Working draft - not for public release 



EPIDEMIOLOGY DIVISION 

DATA SCIENCES DIVISION 

USAF SCHOOL OF AEROSPACE MEDICINE (AFSC) 

BROOKS AIR FORCE BASE. TEXAS 78235 



60 



P.A.NCH KA.-O i: UrDATID ANALYSIS CF LIV?: SlrTH CUTCC'.ES 

1. Introduction 

Since the release of the baseline morblHty report In February 19611, birth 
defects and neonatal deaths reported by study participants during the baseline 
questionnaire have been verified by record review. This verification was ac- 
complished by the review of birth and other medical records, birth certificates 
and death certificates. Verification of negative responses to the birth defect 
and neonatal death questions have not as yet been completed. Reported birth 
defects and neonatal deaths were labelled as belonging to one of nlpe verlfl* 
cation result categories. Table 1 shows the number of reported birth defective 
children and neonatal deaths In each of the nine categories. 



VERIFICATION PROCESS SUMMARY AS OF 15 SEPTF>1BER 198«l 
(Ranch Hand and All Comparisors'* 





Number of 


Number of 


Verification Result 


Birth Defects 


Neonata] 


Deaths 


Cannot locate father 


9 






Records unlocatable 


46 




8 


No care sought 


19 




« 


Refused delivery of records 


31 




* 


Records destroyed 


18 







Confirmed 


231 




56 .. 


Not supported 


23 







Waiting for recorcTs 


1 




6 



For the purpose of data analysis, these nine verification categories were 
collapsed to three for purposes of analysis, as defined In Table 2. 



61 



VERIFICATION PROCESS COLLAPSED DEriNITICHS 



Analytic 

Veriricatton Results Category 

Cannot locate father Unknown 

Records unlocatable Unknown " 

No care sought Unknown 

Refused delivery of records Unknown 

Records destroyed Unknown 

Confirmed Vies 

Not supported . No 

Waiting for records Unknown 



The data analyzed in this report reflect the status of the verification 
process as of 15 September 198U. The date 15 September was chosen Independ- 
ently of the data and was dictated by the logistics of report preparation.' An 
additional Ranch Hand child with Down's syndrome was identified but tour data 
for the father were unavailable at the time of analysis, and this child was 
omitted from these analyses. 

2. Analytic Strategy 

These analyses are directed at testing for the existence of a group by 
verified defect (or neonatal death) by time Interaction. '■'These dataware cate- 
gorized by group (Ranch Hand, Comparison) by verified birth defect (Yes, No) 
and by time of conception (Pre-Southeast Asia [Pre-SEA], Post-SEA).^ ^A _descrlp- 
tlon of a three-way group by defect by time Interaction Is best developed In 
terms of the odds ratio. The "odds" of a birth defect Is a ratio of the prob- 
ability of a defect to the probability of no defect. The ratio of this odds in 
the Ranch Hand group to the corresponding odds In the Comparison group Is 
called the odds ratio. An odds ratio of unity Indicates group equivalence as 
regarding birth defects. An odds ratio greater than unity Is obtained when the 



83-529 95-3 



62 



czCt in Vr.i ?.B.r.cr. -.ar.z rroup i- rreEt=rr -..-.a..-. :-e oitz in ;-■= Corrariicn grou?. 
The odds ratio thus sunxiarlses the group by verified defect associetion. This 
odds ratio niay, however, change with tine of conception (pre-'S£A, posfSEA). 
For example, an odds ratio of unity for pre^SEA conceptions and an odds ratio 
of two for post'SEA conceptions would be suggestive of a herbicide effect. A 
change in the odds ratio with time of conception indicates that the odds ratio 
lo associated with time of conception. Such an association is termed a; three- 
factor interaction by statisticians, the factors being group, verified birth, 
defect and time of conception. 

The preferred statistic in this report Is the test of the hypothesis of no 
three'-factor Interaction. This hypothesis Is equivalent to the statement that 
the odds ratio Is constant with respect to time of conception; I.e., that the 
pre-SEA and posfSEA odds ratios are equal. A p' value for this test less than 
the nominal 0.05 would indicate the presence of a statistically significant 
threcfactor Interaction. In terms of the odds ratio, it would indicate that 
the pre-'SEA and post'SEA odds ratios are significantly different. This test 
for no three'-factor interaction Is, in general, more appropriate than testlna 
for group differences at each level of the third factor. More specifically, 
the test for equality of the pre'SEA and post'SEA odds ratios is entirely fo" 
cused upon whether the odds ratio has changed with time, regarcless of its 
pre'SEA value. Any test on posfSEA data only would assu.-ne that the pre'SEA 
birth experiences of both groups were equivalent, an assumption that appears 
unwarranted In these analyses since the matching variables, paternal age, race 
and military occupation are only weakly associated with the propensity to fa- 
ther birth defective children (Newcombe and Tavendale). These data suggest, in 
fact, that the Ranch Handers and their matched Comparisons are noneculvalent 
groups with the Ranch Handers 'having relatively fewer birth defective children 



63 



prior to service in Vle-.nars thar. do the .Corparlsorj. The test for no threes- 
factor Interaction is, therefore, not only preferred but is the only analysis 
of these data that would account for a possible norequlvalence of these study 
groups prior to their Vletnani experience. 

Consideration of a particular interaction pattern, one that actually ob'' 
tains In these data, illustrates the effectiveness of these analyses; • the 
pattern Is shown In Figure 1. 



Figure 1 



fl HYPOTHETICAL CROUP BY DEFECT BY TIME INTERACTION 




PRE-SEfl POST-SER 

TIME 



Here, both trend lines have a positive slope, as expected, by advancing 
paternal age but they cross over with the rates being different from each 
other, in one direction pre*SEA and in the opposite direction posfSEA. The 



64 



Important point Is not the crossover ?9r se, since any sisniflcanf group by 
defect by tlae Interaction Indicates that the lines differ. The laportant 
point concerns the pattern of switching rat? differences: here the Icwrate 
pre*SEA Ranch Handers have overtaken the hlgh-'rate pre^SEA Comparisons. This 
pattern is reflected in these analyses by a pre^SEA odds ratio less' than' unity 
and a post*SEA odds ratio greater than unity. ' '^ *' 

The power of the test for no three*f2ctor Interaction is'a functlon'of the 
pre-'SEA odds ratio, the post'SEA odds ratio, the numbers of Ranch Hand and 
Cocparlson conceptions pre*SEA and post*SEA, the- number of -defective births 
pre^SEA and posf'SEA and the significance level. Two power curves are shown In 
Figure 2, for the 0.05 significance level and the marginal totals In 'Table 7* 
as a function of the post*SEA odds ratio for each of two values.O.T' and '1 .0, 
of the prcSEA ratio. --•• - 



Figure 2 

POWER OF THE TEST FOR NO THREE FACTOR INTERACTION VERSUS 

THE POST-SEA OOOS RATIO WHEN THE PRE-SEA OOOS RATIOCRl) 

EQUALS UNITY AND 0.7 AND MAROINAL TOTALS ARE THOSE OF TABLE 7 




0.6 1 i.s 

POST-SEA OOOS RATIO 



65 



TMe graph corresponding lo the pre-'ScA oiii- nlio of 0.7 shows the*. ch€ 
power of this test (given the data In Table 7) for detecting a change in the 
odds ratio fron 0.7 to 1.5 is 7C?. Thus. If the true pre and post^StA odds 
ratios are 0.7 and 1.5, this test would correctly reject (at the 55 J?vel of 
significance) the hypothesis of equal pre and post*SEA odds ratios in. ^Of of 
all repetitions of the study. While these power computations apply;, only to 
tables having the marginal totals of Table .7, they do serve to illustrate the 
statistical power characteristics of this study. ,;: 

3. Analysis of Verified Birth Defects .•-..--: 

A summary of the verification process. In terms of counts of children fol* 

lowing the definitions in Table 2, is shown In Table 3. A child with multiple 

defects Is counted only once In Table 3 and the subsequent analyses. For chU* 

dren with multiple verified defects, the most serious birth defect was 

analyzed. In Table 3 and elsewhere in this report, "original" Comparisons 

refer to those 1023 Comparisons who were asked to participate in the baseline 

physical examination before scheduling difficulties arose and. "all" .Comparisons 

refer to the entire cohort of i660 matched Comparisons who received the base* 

line questionnaire. See Chapter V of the baseline morbidity* rebort (Lathrop et 

■ • ; I 

al., 198t)-for a full discussion of these groups. As in the baseline report, 

the primary analyses are those contrasting Ranch Hand children with original 

Comparison children. Contrasts of Ranch Hand and all Comparison children were, 

however, also carried out and are described throughout this. report. 



66 



reble 3 



CHILOREfJ WITH REP0?.T-:D BIRTH DEFECTS 
AHD VERIFICATIOil ??.CCE.-£ RESULTS BY CRC'J? 



Reported as Defective 

Veriricatlon Unverified Missing Data on 

Croup Yes Ho Unknown Total Negatives Questionnaire Total 

Ranch Hand 103 10 57 170 2179 13 2662 

Original Comparison 85 7 H3 135 . 2053 3 2191 " 

All Comparisons 131 9 63 203 3156 13 3377' 

. -.i-.:-:.-:/ -^*^ 
The 26 children with missing rf?crt?d defect status on the questionnaire 

were not Included In the verification process and they still carry a missing 

status. These 26 children with missing questionnaire data were deleted fron 

all analyses. Seven children who were not categorized into one of the nine 

categories shown in Table 1 were ircluded in the "unknown" verification 

status in the subsequent analyses. Two of these were children of original 

Comparisons and five were children of Ranch Handers. The total number of 

children in these tables (2663 ♦ 3377 - 6010) corresponds to the total number 

of live births shown in Figure XI*1 of the baseline mcrbldr.y report. 



Table >; displays the verification status of reported birth defects by gen* 
eral categor ■ of the defect. The results of the verification process for 
specific defects by group and severity clessif Icatlon are contained in Appendix 
Table 1. 



67 






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mm - « eg 



70 



As in irr tiS'iline rtzcri, '.r.ly thcs? ■;^rif:i't zir:'r: Crfr^ts ss^isr/in^ ir.e 
definition riven In Appendix V of the baseline report are analyzed. Tail': 5 
shows the counts of the children In Table 3 having verified birth- defects with-" 
in the definition by time of conception (pre*SEA, post'S£A), verification 
results (Yes, No, Unknown) and group (Ranch Hand, Original Cowparison, All 
Comparisons). As previously noted, one Ranch Hand child with a verified con* 
finned birth defect cogld not be classified by tine of conception because tour 
data for his father are missing. 

Table 5 : . .,. 

CHILDREN WITH MULTIPLE BIRTH DEFECTS 



Pre'SEA 



Post'SEA 



Ranch Hand 

Number of children 

Number of conditions reported 

Number of conditions verified 

Original Comparison 

Number of children 

Number of conditions reported 

Number of conditions verified 

All Comparisons 

Number of children 

Number of conditions reported 

Number of conditions verified 



s 


K 


L 


s 


M 


L 


10 


3 





8 


5 


1 
2 


22 


8 





13 


16 


8 


17 


2 





13 


12 


5 


7 


1 





3 


5 





12 


5 





6 


9 


1 


10 


2 





6 


7 





8 


2 


1 


1 

5 


8 





l«l 


8 


1 


11 


15 


2 


12 


n 





1 9 ■ 


13 


1 



Table 5 shows the number of children In each group reported to have multl-' 
pie birth defects and the verification status of these defects. If a child had 
defects with differing severity, the child .was placed in the category of 
his/her most severe defect. 



71 



TaDle c 

CROSS TABULATION OF CHILDPFIN HAVING REPCPTED 21P.TH DEFECTS 
SATISFYIHC THE OEFirilTIO?! 



Pre*SEA Post'SEA Totals 



Croup Yea No Unknown Yes No Unknown Pre-^SEA Po9t*SEA 

Ranch Hand «I7 2 11 56 9 15 90 80 

Original Comparison 53 »< 30 32 3 13 87 ^8 

All Comparisons 73 5 t5 58 • U 22 • 123 8U 

The totals In Table 6, together with the Ranch Hand and all Comparison 
children with no time of conception information, are slightly different from 
those totals shown in Table XI*10 of the baseline report, because Table XI*10 
contains data that were not analyzed in the baseline report. The counts, in 
Table 6 do account for all children having reported birth defects within the 
definition and reflect minor numeric changes due to the verification process. 

Following the format of the baseline report, these analyses are focused on 
the Ranch Handers and the original Comparisons. While these contrasts are of 
primary importance, corresponding Ranch Hand versus all Comparison contrasts 
are shown in the Appendix. The subject of these statistical investigations is 
the change, if any, in the group (Ranch Hand, Original Comparison) by verified 
birth defect relationship with respect to the time of conception as pre*SEA or 
post* SEA. 

A statistical assessRent of the Ranch Hand and original Comparison data 
with a dlchotomous response (unknown, not unknown) did not reveal any signifl* 
cant difference in the pattern of verification between the groups (p - 0.65), 
adjusted for time of conception.' The corresponding analysis of the Ranch Hand 
and all Comparison data gave 'a similar result (p • 0.71). Thus, patterns of 



72 



false positive repor'.;r.c do nc. sppesr '.c 'Jirfc.- Setwesr. :.-r grcuos. Sir.ce 
there Is no association In thes* tfata betveen groups and "unVnown" veplflcatlon 
status, the children having un'Knowr. verification status have been- removed fror 
subsequent analyses. Verification of birth defects, therefore, has only two 
values (yes, no). These data, with unknowns rer:.oved, are sutcmarized In 
Table 7. 



CKILDREM WITH VERIFIED 5ISTK DEFiCTS WITHIN THE DEFI.VITIOM 

BY VERIFICATION OUTCOME, GROUP Ai'.D TIME •- • 

Pre^SEA (%) Post'SEA CO ' 

Group Yes No Yes Ho 

Ranch Hand H7 (2.8) 1630 (97.2) 56 (6.3) 838 (93.7)" 

Original Comparisons 53 (3.8) 1351 (?6.2) 32 C.i^) 697 (95.6) 

The p-'value for the test of the hypothesis of no group by defect by time In 
these data Is 0.02H. This Implies that the pre-'SEA odds ratio for verified 
birth defects, 0.73, Is significantly different from the post*£EA odds ratio, 
l.'<6, for contrasting Ranch Handers and original Comparisons (p • 0.021)). The 
equivalent analysis using the data from all Comparisons (Appendix Table 2) 
resulted in a similar finding (p • 0.023). 

As reported In the baseline report, an analysis on reported defects, ignor* 
Ing the verification results, shows a significant three-'way reported defect by 
group by time Interaction (p ■ 0.0!-'7), with odds ratios changing from 0.85 to 
1.39. • 



73 



TaSle X>1-- c;" ir.s :££-:l:r,€ repc.-t sr.c-.s cc'-.'.-vS , ;u-. r.o s.'. = lysi£. o:" re^^ 
ported birth defective c^.ildren by group (Ranch Hand, original Comparisons), by 
occupation (cfflcer, enlisted flying, enlisted ground) and by time of concep-' 
tion. Table 8 shows the corresponding counts of children by birth defect 
verification outcome (yes, no). 

Table 8 
CHILDREN WITH VERIFIED BIRTH DEFECTS BY OCCUPATICriAL GROUP AND TIME 

Occupa" Pre--SEA ('.) ' ' PosfSEA (*,) 

tion Croup Yes No Yes No 

Officer Ranch Hand 2H (3.0) 77K (97.0) 9 (3.9) 221 (96.1) 

Original Comparisons 27 (3.9) 671* (96.1) 12 (5.2) 215 (91.7) 

Flying ■ Ranch Hand 6 (1.7) 3H5 (98.3) 9 (8.7) 95 (9^.3) 

Enlisted Original Comparisons 11 (3.5) 3C7 (96.5) ^ (3.5) 102 (96.2) 

Ground Ranch Hand 17 (3.2) 511 (96.8) 38 (6.8) . 52? (93-2) 

Enlisted Original Comparisons 15 (3-9) 370 (96.1) 16 (U.O) 3P0 (95.0) 

Log*linear analyses of the data in Table 8 show no significant four-'way, 
group by defect by time by occupation, interaction (p - 0.20). This lack of 
four-'way interaction allows consideration of a test for the threcway interac* 
tion of interest (defect by group by time) adjusted for occupation. This test 
gives a p'value of O.O61. These findings suggest that the pro'SEA odds ratio 
and post-SEA odds ratio are only borderline significantly different, when ad" 
justment for occupation is performed. Similar analyses of the data from the 
total Comparison group revealed equivalent results (Appendix Table 3). Here, 
and elsewhere In this report, adjustments for covarlates are carried out to 
reduce bias in the analysis. The price for this reduction. In the absence of 
more data, is a loss in precision. Hence, the- slightly increased p-'value of 
0.061, as compared with the unadjusted value, 0.021, reflects either true ab" 
sence of a three*way (defect by time by group) Interaction or a reduced ability.. 



74 



to ce-.ect s '..•*■-•= :-..-'.■••-•.■;;.' ir.- r.-ac.i.r cue :c ir. ir.cr^ijc". r.--ot.- cf cells -iih 
a fixed data base. A distinction between these V«o alterratlves (a cruie ansl' 
ysls with mere potential bias and better power cr a refined aralyzls with l.ss 
bias but with lower power) can not be made .vithout rore data or more refined 
statistical proccrtures. 

An analysis of the data In Table 7, adjusted for four covarlates (mother's 
smoking and drinking during pregnancy, nother's age at conception and father's 
age at conception), was carried cut. Tr.e tnree'^vsy Interaction (croup by de* 
feet by tine), adjusted for mother's smoklnc, drinking end cffe and father's 
age. Is borderline statistically significant In the full analysis (p - 0.072). 
Equivalent statistical testing with the data from the total Comparison group 
resulted in similar findings (p - 0.06), and these results are shown in Appen-' 
dix Table H. 

Table 9 

CHILOREN WITH VERIFIED BIF.TH DEFECTS 

BY CROUP, TIME OF CONCEPTION' A>JD VERIFICATION OUTCOKE, 

WITH BOTH PAREi.TS UNDER 35 AT CONCEPTION ANC- 

MOTHERS WHO DID HOT DRINK ALCOHOL DURING PrHIGNANCY 

A. Mothers not s-noklng during pregnancy . 

Pre--SEA CO Posf'SEA (',) 

Group Yes No Yes No 

Ranch Hand 25 (3-0) 8l8 (97.0) 28 (5.1) «)93 (91.6) 

Original Comparisons 2U (3-1) Ti2 (96.-») 20 (5.C) J.'.O (?5.C) 

B. Mothers sacking during pregnancy . 

Pre-SEA (?) Po;t"SEA (?) 

Group Yes No Yes No 

Ranch Hand 12(^.1) 379(96.9) 11 (8.1) 125 (91 .9) ' ' 

Crlglnal Cor-parisons 19 (6.3) 2S2 (93.7) U (?.3) I'o (96.7) ' 



75 



The fully cCJjsteO inelysi: Just cJescrl&ed Is subject to criticise because 
of the many empty cells In the full contingency table. In the above analyses, 
2530 (60.65) of the i«178 children of Ranch Handers and original Cccparisons 
were offspring of mothers who did not drink or smoke during pregnancy and were 
under 35 at time of conception and of fathers who were under 35 at conception; 
9U8 (22.7?) of these children had mothers who smoked and did not drink during 
pregnancy and were under 35 at time of conception and. had fathers who were 
under 35 at conception. A summary of the data in these two categories of co' 
variate values is shown in Table 9. Account of the structure cf the full table 
would then be taken by separate analyses within each of the two arrays shown in. 
Table 9. These analyses were accomplished. There is a significant four^'way 
interaction in the data shown in Table 9 (p - 0.051), indicating that three-way 
interaction of interest (group by difect by time) changes with maternal smoking 
habits. The corresponding four'way interaction in the Ranch Mand versus all 
Comparison data was not significant (p - C.13). Analyses within parts A and 3 
of Table 9 were then carried out. The threCway interaction (group by defect 
by time) is not significant in the data of part A of Table 9 (mother not smok-' 
ing during pregnancy). However, this three^'way interaction is statistically 
significant (p - 0.012) in the data of part B of Table 9 (mother smoking during 
pregnancy); the odds ratio changes from 0.H7 to 2.55. In summary, there is an 
Indication that smoking by the wife of a Ranch Hander during pregnancy is asso* 
ciated with a Ranch Hand versus Comparison differential in birth defects over 
time of conception (p - 0.051). 

Counts of verified birth defective children by severity of defect (light, 
medium, severe), group (Ranch Hand, original Comparison) and time of conception 
(prcSEA, post-'SEA) are shown in Table 10. The definition of severity is. taken 
from the baseline report and 'is shown below; 



76 



Severe: Conditions which are life threatening or produce severe 
handicaps (e.g., physical, mental, motor). 

Moderate: Conditions which are not life threatening and handicaps 
which, with medical care, will not interfere with the individual's 
overall health or socioeconomic progress. ^.■__. 

Limited: All conditions which, without medical care, would not in* 
terfere with the individual's health or socioeconoolc progress. 



CHILDREN WITH VERIFIED BIRTH DEFECTS 
BY SEVERITY. CROUP AND TIME OF CONCEPTION' 







Defective 




Not 


Croup 


Light 


Moderate 


Severe 


Defective 


Ranch Hand 
Original Comparison 


12 


1J» 
16 


30 
12 


838 
697 


Ranch Hand 
Original Comparison 


2 

1 


13 
15 


32 

37 


1630 
1351 



Time 
PosfSEA 



A log-'llnear analysis of the data in Table 10 re.ealt-d a borderline grcip 
by severity by time of conception interaction (p - 0.05). An analysis llmltetf 
to the children with verified defects, categorized as light, moderate or se* 
vere, showed no statistically significant group by severity by time vT 
conception interaction (p - 0.29). The corresponding analyses with all Coot* 
parisons also revealed no significant three-'way interaction (p - 0.13 amt 
p - 0.61), respectively). These results are displayed in Appendix Table 5.. 



77 



T-o 'iata-'Cf ?e-.C5n: ir.slyses (pes", hoc) wer» slso c:n't^jc*.rr c- '.'r.e Ci'.t ir. 
Table 10. First, children classified as having llsilted birth defects were re* 
classified as "not defective," leaving only two categories of defective 
c'llldren, moderate and severe. In the analysis. The results of this analysis 
revealed a statistically significant group by defect by time interaction 
(p - O.O'i). Second, children classified as having United or moderate birth 
defects were reclassified as "not defective," leaving only the severe category 
of defective children in the analysis. The results of this analysis revealed a 
statistically significant group by defect by time interaction (p ■ 0.01), with 
the odds ratio changing from 0.72 to 2.07. These analyses suggest that the 
three-way interaction found in Table 7 does not depend on severity of defect. 
The corresponding analyses were also carried out on all of the data, shown in 
Appendix Table 6; the results were similar, with the respective p*values being 
0.09 and 0.01. These post hoc analyses are of secondary importance relative to 
the primary analyses shown elsewhere in this report. 

Counts of verified birth defective Ranch Hand children conceived after the 
father's duty In Southeast Asia are shown in Table 11 according to their 
father's occupation (officer, flying enlisted, ground enlisted) and estimate of 
herbicide exposure (low, medium, high). 



CHILDREN WITH VERIFIED BIRTH DEFECTS 
POST*SEA RANCH HAJ.'D BY FATHER'S OCCUPATION AND HERBICIDE EXPOSURE 



Officer (i) Flylnc Enl (j) Ground Enl (i) 

Exposure Yes No Yes No Yes No 

Low 3 (14,0) 72 (96.0) (0.0) 29 (100) 11 (1.6) 165 (93.1) 

Medium H (7.1) 52 (92.9) 1 (12.5) 23 (37.5) 11 («>.?) 211 (95.1) 

High 1 (1.2) 83 (98.3) 5 (11.1) 39 (88.6) 16 (10. 3) 1 1? (89.7) 



78 



Statistical analyies of the <;ata in Table 11 were restricted to the en* 
listed ground cohort <i>:e to low counts In the officer and flying enlirted data. 
Analyses within the e'"oun<^ enlisted cohort on the occurrence of birth defective 
children and herbicide exposure were carried out using each of the four covari* 
ates, one at a time. These four analyses are sununarized in Table 12. No 
significant relationships between the occurrence of birth defective children 
and herbicide exposure, adjusted for these covariates, were seen in these data. 



EXPOSURE ANALYSIS BY CHILDREN WITH VERIFIED BIRTH DEFECT 
(Ranch Hand Enlisted Ground Personnel Only) 







P'Va: 


lues 


for 






Covarlate 


No 
Cc 


Defect by Exposure i 
ivariate Interaction 


tjy 


No Defect by 
Exposure Interaction 


Mother s.-noking 




0.59 










0.25 


Mother drinking 




0.89 










0.20 


Mother's age 




0.35 










0.2JJ 


Father's age 




0.65 










0.21 


Neonatal Death 


Analysis 















Verification of reported neor.atal deaths was also accomplished during the 
same time period, and the data are summarized in Table 13. 



79 



REPCSTED KEOMATAL DEATHS 
AND VERIrlCATIOM PROCESS RESULTS Sr CSOU? 



Positive Responses 

Croup Verified Unverified Total 

Ranch Hand 31 9 "(O 

Original Comparison 17 " 21 



Negative Responses Total 
2623 2663 
2170 2191 



These data are shown in Table It, by time of conception (pre*SEA, post* 
SEA), verified neonatal death (Yes, i'.o) and group (P.anch Hand, Orljlnal Con" 
pari son). 



VERIFIED NEONATAL DEATHS BY TIME AMD CP.OUP 
(p - 0.0378) 



Croup 

Ranch Hand 
Original Comparison 



Pre-SEA (i) 
Yes No 

18 (1.0) 1705 (99.0) 

15 (1.0) 1120 (99.0) 



Post'SEA (<) 
Yes No 

12 (1.3) 905 (98.7) 

1 (0.3) 7U3 (99.7) 



A log*linear analysis of the data in Table 11, unadjusted for other covari* 
ates, shows a significant three-way (group, by time by neonatal death) 
interaction (p « O.Oil). In other words, the pre'SEA odds ratlo,^ 1.00, is slg* 
nlflcantly different from the post'^SEA odds ratio of 9.85. A parallel analysis 
on verified data from all Comparisons gave similar results with a significant 
change (p < 0.01) in the odds ratio from 0.93 to 8.67. A corresponding analy* 
sis using unverified data from original Comparisons In the baseline morbidity 
report resulted in a borderline significant finding (p - 0.09), with the pre 
and post'SEA odds ratios being 1.23 and 3.93. When the unverified data from 



80 



line total Ccrpa.-iscn r-:-: 'c.-i ri.nali plus nola-.t-ir.'.:) vsr^ jse.: in the base" 
line morSldity report, a statistically significant result was obtained 
(p S 0.01), with t'nc pre anri post'SEA odds ratios of l.06 ann 5.06.. 

The neonatal death data are too sparse to permit a meaningful analysis 
stratified on the exposure index or other covariates. 

5. Conclusions 

Birth defects and neonatal deaths reported by study participants during the 

... • .'■■■• ■» ', 

administration of the questionnaire phase of the baseline study have been sub* 
Jected to verification based upon birth/death certificates and medical records- 
The results of the verification process are summarized in the following two 
fables. 

Table 15 
VERIFICATION STATUS OF CHILDREN WITH REPORTED BIRTH DEFECTS BY GROUP 



Croup 


Number Reported 


Obtained 


Number 


Verified 


Verified 


Ranch Hand 


171 


118 




103 


60.6 


Original Comparisons 


135 


101 




85 


63.0 


All Comparisons 


208 


15« 




131 


63.0 



81 



Table 16 
VERIFICATION STATUS OF REPORTED NEONATAL DEATHS 3Y GROUP 



Croup 


Nunber Reoorted 


Nunber 


Verified 


Verified 


Ranch Hand 


140 




31 


77.5 


Original Comparisons 


20 




16 


80.0 


All Comparisons 


32 




26 


81.3 



In spite of extensive efforts, some records were unobtainable and their 
receipt is not anticipated. The verification of positive reports of these 
conditions were not statistically different in the three groups. Thus, differ* 
entlal reporting of positive responses to the birth defect and neonatal death 
questions does not create a detectable bias In these data. 

Statistical analyses comparable to the analyses on reported but unverified 
data in the baseline report were conducted, and similar findings were observed. 
There was an increase in the risk of Ranch Hand birth defects with time (pre 
versus post*Southeast Asia), and this change is statistically significart. 
These data were also stratified on the smoking history of the mother during the 
pregnancy In question. There were no group differences in birth defects among 
those women who did not smoke; however, there was a significant change in risk 
of birth defects with time among Ranch Hand children born to mothers who did 
smoke during pregnancy. 

The herbicide exposure index was applied to these data, but the number of 
defects among the relatively small strata of officers and enlisted flyers made 
a meaningful analysis Impossible. However, the larger group of ground enlisted 
personnel was- large enough to permit this analysis. This analysis did not 



82 



reveil i.- siscciaticr b»-.weer. ^.e-sicice Txpcsuri anO f".e occur .-i.-ice c:" iir-.r 
defects. The exposure Index used In this report Is a theaterwide estlaste of 
exposure and is not Indlvldual-'speciric and needs further refinement. 

The neonatal death data were also reanalyzec. A significant change In risk 
of the occurrence of neonatal death with time was noted; however, this is due 
In part to an obvious decrease with tine in neonatal deaths born to Conparl" 
sons' wives. The Ranch Hand rate was stable with time. ' These analyses were, 
however, unadjusted for maternal age at time of conception. Additional ad* 
Justed analyses will be carried In future updates or other socloecononilc 
variables of possible importance. 

The reanalysis of these data corroborated the findings of the baseline 
report; however, once again, no consistent relationship to exposure was cb" 
served. The next step in the full analysis of these data is to verity the 
negative reports to complete the assessment of differencial reporting. It is 
anticipated that another 12 months will be required to complete the ccllection 
of medical records on the more than 6000 live births reported by the study 
participants. 



83 



Appendix Table 1 

AN/LYZBD PAXH HA^D 

SEVERE 



FRE'SEIA 

Not Not 
ICD Re' Va-l" Sep* Veri" 
OOOE ported fled ported flable 



fOIEMCUTURE 



POST'SEA 

Not hiot 
RC Ve-1' Slp* Vq-I' 
crrted Tied ported flable 



22801 



7K190 

7U23 
7')259 

7«29 

7'J511 
7'<5^ 
7155 
71^59 

7'i602 
71666 
71639 

7169 

7170 

71721 

71722 

7173 

7155 

71900 
71910 
71920 
7503 
7505 
7511 

75161 
7519 

7530 
7533 



2 


2 






2 

1 

1 


2 

1 




1 


1 
3 






1 


1 
3 

1 








2 








2 
1 








14 
1 


2 

1 




2 

1 


3 


1 

1 

2 


1 





Hemangioma of skin and 

subcutaneous tissue 
Spina bifida with hydrooe* 

phalus 
Spina bifida without hydroce* 

phalus 
Hydrocephalus 
Other specified anomalies of 

spinal oord 
Unspecified ancrraly of brain, 

spiral cord 
Absence of ear 

DoOjle outlet rl^it ventricle 
Ventricular septal defect 
Atrial septal defect 
Unspecified defect of septal 

closure 

Pulinonary valve stenosis 
Congonital heart block 
Other specified ancrralies, 

heart 

Unspecified ancmaly of heart 
Patent ductus arta-iosus 
Anoialies of aortic arch 
Atresia i stenosis of aorta 
Ancnalies of pulmonary artery 
Agenesis, hypoplasia, dyspla- 
sia of ling 
Cleft palate 
Qeft lip 

Cleft palate with cleft lip 
TVacheoesophageal fistula 
Pyloric stenosis 
Atresia i stenosis of small 

intestine 
Biliary atresia 
Unspecified anardy of dlges 

tlve system 
Renal agoiesls & dysgenesis 
■ether specified anxalles of 

kiOTey 





2 






2 


1 




1 













3 




2 


? 






1 
1 

1 


1 



84 



prevrix Tib:- l (Zc'.-.'c) 

AMALYZED W.'irH KVT- 

?r/ERE 



FRE-SEA 

Not Not 
ICD Re* Veri-' Sip* Veri" 
POPE ported fled pcrted Tlable 



rCME>CUTlJRE 



PCST'SEA 

Not Not 
Rs* Ve-i' Sep* Verl* 
corted fled ported flable 



7534 


1 


1 






7539 


3 


1 




2 


75^(61 
75'<70 
75U79 
75529 


1 
2 
1 


1 




2 


75583 


1 


1 






7560 










75610 

75615 
7580 
7^1 
7598 


] 


\ 




1 



Othar specified aronalles of 

ireter 
Unspecified araraly of iri* 

nary system 
Congenital pes planus 
Cefonnlty foot, >DS, clubfoot 
Other cteformlty of foot 
Longitudinal deficiency 

phalanges 
Other congenital deformity 

hip (joint) 
Ancnalles of skull i faoe 

txjnes 
.Ancraly of spine 
Fusion of spine 
Down's syndrcme 
Anomalies of adrenal gland 
Other specified araralles 



2 2 

1 - 1 

2 2 

2 2 



85 



Ap?eic!ix Tcole l (.Ccr.t'C) 

AMALYZBD PA'C^ HAND 

^C)OERATE 



PRE'SEA 

NoC Not 
Re* yeri'- Sup* Va-i* 
ported ried pcrted riable 



hOfBCUTURE 



POST'SEA 

Not tot 
Re» Verl" Sup' Ve-i* 
ported fled ported flable 



22800 

5531 

7M38 


2 

3 
3 


1 




1 

3 
2 


THiKX) 


1 


1 






71U21 
71129 

7LlJ"3 


1 


1 






7508 










75219 










7525 


2 






2 

1 


(5cu 

7531 
7538 


, 








7510 


1 




1 




7512 


3 


2 




1 


75130 
75150 
75153 
75161 
75170 
75131 
75189 


2 
1 


1 

1 




2 


75501 
75502 
75513 


1 






1 


7K63 
75566 
75567 


3 
2 

1 


3 




2 

1 


75569 











HemanglcR-a, unspecified site 

linbillcal hernia 

Othar specified aramalles of 

the eye 
Unspecified anaraly ear with 

hearing LTipairoient 
Absenoe of the ear lobe 
Other ancmalies of the ear 
Unspecified anomaly of the 

ear 
Other specified araialies, 

upper alunentary tract 
Other ancmalies, fenale 

geiitalia 

Undescetidc-d testicle 
Hypospadias 
Cystic kidney disease 
Other specified anorralles 

of bladder and urethra 
K\sculoskeletal defcrmity, 

skull, face, jaw 
Musculoskeletal deformity, 

spine 

Dislocation, hip, inilateral 
Talipes varuses 
hbtatarsus varus 
Pes planus 

Deformity of foot, NOS 
Pectus excavatun 
Other specified, nonterato^ 

gcnlc anaialies 
Polydactyly, fingers < 
Polydactyly of toes 
Syndactyly, toes without 

fUSlOTi 

Deformity of hip (joint) 
Other aranalies of the toes 
Other anomalies of the foot, 

NBC 
Other anomalies of. the lowe* 

limb 



2 2 

1 1 

1 1 

1 1 

1 1 

1 1 

3 1 



•.poenclix Ta:.-? ; C-:-.t 
ANALYZED R;;)Ci ^.-IZ 
f-COEBATE 



Id) 

ODOE 


Re- 
ported 


mE-SEA 

^tot 
Veri- Slp' 
fled ported 


tot 

Ve-i' 

riable 


7560 


1 






1 


75689 


' 


' 






7569 










75733 










7575 











NQ-eJCUTURE 



FOST-SEA 

K'ot Not 
Re- Va-i* Sup* Veri' 
ported fled ported flable 



Amnalles of the sl<ull & 

face bones 
Other ancnalies, roiscle, 

tendons, fascia, ccmective 

tissue 
Other i unscecifled ancralies 

injsculoskeletal system 
Pigmentary anotialles of the 

skin 
Specified anomalies of the 

nails 



87 



Acp-^dix TaSle l (Ccr.fd) 
ANALYZED RAi'CK HA'O 



PRE'SEA 

Not Not 
ICD Re* Veri" Sip* Ve-1* 
CODE ported fled ported flable 



NaiENCLATURE 



POST'SEA 

Not tot 
Re* Ve-1* Slp* Va-i* 
ported fled ported flable 



2169 


1 


1 






7K38 










70361 
7U689 


1 






1 


ime 










7500 
75010 
75019 
75^50 
751^60 
75H70 
75^79 


1 






1 


75511 










75513 
75560 


1 
1 


1 




1 



Ber^gn neoplasm, skin, site 

inspecifled 
Othar specified aramaly of 

eye 
Ptosis 
Other specified anon^les 

of heart 
Other ancnalles, peripheral 

vascular system 
Tongue tie 

Anomaly of ton^je unspecified 
Other anoralles of tongue 
Talipes varus 
Talipes valpjs 
Dc-ronmli;.' feet ^CS 
Other specified deformity 

of feet 
Syndactyly finge-s without 

fusion 
Syndactyly tee with fusion 
Unspecified ancttaly lo-y 

llrrfc 



88 



:<r.c:x Ti^le 1 (Cc-.t'i) 

A.MALY2ED HXCH H.-:D 

QMITED 



PRE^SEA 

Not Not 
ICD Re* Ve-i* Sup^ Veri* 
OOOE ported fled ported flable 



NCf-BCUTVJRE 



ros-.^SEA 

Not Not 
Re* Va-1* SlV Ve-1* 
ported fled ported flable 



75567 
75569 










75732 
75733 
75739 


1 






1 


7576 


1 






1 



Anotialles of foot. NBC 


1 






1 


Othe- specified ancraiy lo-(e- 


1 • 






1 


limb 










HamartOTBS 


5 


2 


1 


2 


Plgrentary ancrralles of s:<in 


2 


' 1 




1 


Other specified ancralles, 


2 


1 




1 


Skin 










Other specified o.-)c«ralIes 


1 




1 




breast 











Appendix TsSle 2 

VERIFIED SIRTH DEFECTIVE CHILDRm 
WITHIN THE DFrlNITIOH BY VEP.IFICATIOIJ OUTCC.XE, CPO'JP, TIME 



Croup 
Ranch Hand 
All Comparisons 



Pre^SEA (J) 
Yes No 

H7 (2.8) 1630 (97.2) 

73 (3.7) 1922 (96.3) 



Post'SEA (?) 
Yes No 

56 (6.3) 638 (93.7) 

58 (1.5) 1218 (95.5) 



Acser.cix 



iole 2 



VERIFIED EISTH DEFECTIVE CHILDRE?! 

BY GROUP OCCUPATIOM AMD TIME 

(All Comoarlsons) 



Occupa* 


Group* 


Pre*SEA 


(5) 


Post" 
Yes 


SEA (?) 


tlon 


Yes 


No 


No 


orricer 


RH 
AC 


2i< (3.0) 
36 (3.8) 


77U (97.0) 
911 (:''.2) 


9 (3.9) 
18 (1.5) 


221 (96.1) 
378 (95.5) 


Fly Enl 


RH 
AC 


6 (1.7) 
H (3.5) 


315 (98.3) 
390 (96.5) 


9 (8.7) 
8 (5.9) 


95 (91.3) 

128 (g'*.!) 


end Enl 


RH 
AC 


17 (3.2) 
23 (3.6) 


511 (96.8) 
621 (96.1) 


38 (6.8) 
32 (1.3) 


522 (93.2) 
722 (95.7) 



(•RH - Ranch Hand, AC - All Comparisons) 



90 



:er.di:< Tc5le « 



VERIFIED BiaTH DEFECTIVE CHILDREN 

BY CROUP. TIME OF COHCEPTIGM AMD VERIFICA7ICM OUTCOME, 

WITH BOTH PAREHT3 UNDER 35 AT COKCEPTICN .VID 

MOTHERS WHO DID HOT DRINK ALCOHOL DURING PRECNAJICY 



A. Mothers not smoking during pregnancy . 

Pre^SEA ii) 
Croup Yes No 

Ranch Hand 25 (3-0) 8l8 (97.0) 

All Comparisons 39 (3.5) 106l (96.5) 



Posf^SEA (<) 
Yes No 

28 (5.1) t93 (91.6) 

37 (5.2) 676 (9H.8) 





Pre- 


SEA (?) 


Croup 


Yes 


No 


Ranch Hand 


12 (3.1) 


379 (96.9) 


All Comparisons 


22 (5.6) 


371 (9U.H) 

/'. ooenCix TeM 



Post' 


SEA 


CO 


Yes 




No 


11 (8.1) 




25 (91.9) 


8 («.") 




173 (95.6) 



VERIFIED DEFECTIVE CHI LORE:.' 
BY SEVERITY. GROUP A.MD TIME OF COHCEPTICM 





Croup 


Not 
Defective 




Defective (.'.) 




Time 


Light 


Moderate 


Severe 


Post*SEA 


RH 
AC 


838 
1218 


12 (21.1) 
9 (15.5) 


11 (25.0) 
21 (11.1) 


30 (53.6) 
25 (13.1) 


Pre-SEA 


RH 
AC 


1630 
1922 


2 (1.3) 

3 (1.1) 


13 (27.7) 
23 (31.5) 


32 (68.1) 
17 (61.1) 



Aocendix Taile 5 



VE.SIFIED NEONATAL DEATHS 
BY TIME AND CROUP 



Pre-'SEA ('. 



Croup Yes No 

Ranch Hand 18 (1.0) 1705 (99.0) 
All Comparisons 23 (l.i) 2019 (98.9) 



Post-SEA (?) 
Yes Ho 

12 (1.3) 905 (%B.7) 

2 (0.2) 1307 (99.8) 



91 













t* — = t i =^ 






.^ 



> c 



92 



Study disputes exposure, 
Agent Orange death rates 



C ontinued (rom Pag* 1-A 
fiugv report f tfx 
p<irto<l I hat I he c.^p 



THll^^^ y kin ranr cr. 



lli:itjl]ijalrs' g" "'y >'^'< ili-li'rniim.tl 

irii'ri' wns "no..(U ffi,'n!iirc" hclvvt'cn 
fnr~iwii p^min>v uiwn iipiv inajor 

liji1Trn.lLtls wiTP I nn^sjili-ryil 

AniiihiT ruunil ol |(h\sical cxaini- 
niiliiMis (nr Ihi' two CTOHpf Ix-Kiilt lit 
May ami aiv scliwliiiuil (or vniiipU- 
liiiii in Marr!) 

WvUv salil thai llif IHSTiM ciiM ol 
I III- vliiily. iK-vaiiM- private tiniis aiv 
uniliT uinliaci In |KTlorm Ihi* exam- 
iii:iliiii)... cuin|iilo ilala and niakv suiv 
X <•%.•;. is alxMil ?■-'■-' -i millliMi. 

Stum- 23 lo 30 KpldcmloloKy DMs- 
mil iHTsonnvl al RnKiks arc iimnllnr- 
In;: the Mudy. scln-dulvil to run until 
■.'wr.'. 

riHr saiil ihal n-M-MKlHTs tiir - 




__ issWe. he e x plained. Iha 
Uic cipo .vd croujJaicr 

bir1h dcrcrUi ihn t ar cn'l . -^ 

■"iiiKrrd.defcas by pa rcnU \n ihe iin- 

t'jifr^HM LTUUn. 

Wolu- said IhnI some of Ihe Air 
f'liriT im-n Ix-ing studied "were 1.00(1 
llini'.s more expos'.xl (In Aeenl Or- 
aiiuf) ihan cround forces In a rtlretl 
spray paili-m on a ime-limc liasl.v" 

liullcis ruptured lanii.s hnlilln*; Ihe 
< hemical. he sjild. and malnlciihnce 
iTi'ws were "kni-eling in Ihe Mulf lo 
repair Ihe damaue. 

Ill- aildcd that the cliemical 
wnrlii'd well lo clean off greasu and 
nirn ••rleiininl llH-lr Ivxruii «illl ii." 
IIk* Miljsianei" U "ab.snibiil \crj rap- 
iillv lhriiiit!h Ihe .-(liui." hv iMrtiil.' 

Al ll«- Iwlfhl of ils use. tViilie .>mlil. 
:i:i nr .« ain-ralt »viv spruyinj; the 



di-fnllpnl on a dally basis. 

Air crews alto were exposed lo 
Ihe spray, he said, since side iloors 
nonnallv wore left open lo reduce 
IIh! Ileal and cockpit windows were 
left open In lessi-n the chance of In- 
juiv from windo-.v Irapmrnl.s. 

the spray inn pioyrain wa.< dub- 
bill n|M-ralinn llanch llaiHl, sn llie 
siitilv uas nami-d ()|K-ralivn llanch 
llanil II. 

The lali-yt sindv rvpnrt comes af- 
ter a IIWJ million selll.-minl liy 
clH-miral conip:mii-s Ihal n)a<le IIk- 
iM-rbiclde was approietl early Ibis 
\i-:ir. More lhan ItiU.aiiil wleiao.i 
iiti-d claiiivs fur Ihi- mnni-y. with 
.some 4.iiiiV Texans iilinc the largiexl 
numlK-r. 

Wolfe said thai Ihe eomiianles 
may have sellleil lo avoUt Ihc toMs 
1)1 li'H(.1hy l|li|;alliin. 

AI.SO. t're.sideiil Iteapan .sij.'netl a 

Inll In dclobir Ihal provldi-s lempu- 

rarj' ciiin|)ens:itiiiM for I wo \i-ur.N lo 

\elrraii.s who have drveinpi-d n skin 

coneiu.slvely linkiil lo Agent 



verc facial condition called chlor- 
aenc. • was nol prewnl In Ihc Air 
Knrcc men exposed. He saiil Ihal the 
skin erupt loiK, which aren't lalal. are 
prrdominalely found aoionp |>eoble 
Mho were exposed durinc Indusfriiil 
occidcnis involvlnp the herbicide. ' 

Mortality figures ri'least-d _\)i|h 
the latest fepoit show 55 ik-alh-rCW 
percenl) among Ihe Itanch ll^d 
pcr.sonnel anil 2)0 dealh.s (-t.6 per- 
cent i ainnni; the 6.171 men In Ihe 
cimipailsiin prniii). 

Aci'ordinp In the inorlallly rale of 
Ihe general U.S. Anglo male iMipula- 
lion. Wolfe added, there shotilil lia\e 
been u\m\l BO deal lis |T |K-ri-enl) 
ainnnp An^la men ex|<nsed to Ai^-eiil 
OraiiKi' Insle'ad i-f Ihe SI IIkiI o«- 
i-umnl 

\ jOwI* of Army am^ Marim- |iir 
simiM-l wImi wi-it •■\|ins«il l«i .\»;eii< 
Oranin- i.s Ju.sl bi-Ktnnui(!. 



93 



DEPARTMENT OF THE AIR FOR^T^i^TT/'Q^J^y^^ 



^^^•.K//Va USAf SCHOOL Of At«OSfACI XtOlCIHt 

l^^ifc^'ia »»00ltJ Al« fOKCt lASt. TEXAS 'fzjs/ / ^ 



Honorable Thomas Daschle RECEIVED OCT 1 9 1987 

United States Senate « ■ o wo< 

Washington DC 20S10-0001 

Dear Senator Daschle 

In response to your recent letter concerning the Air Force epidemiologic 
study of the health e ffect s of Agent Orange, 'Dr^glSBlghalelCT-DrT^ichard •" 

Ai b¥n«6;gtjagj!ffivpillwr^a3^^ 

■s(«cTiflc35ues33pn^ Dr Albanese was a study principal investigator from 
1978 to 1984. Or'joel Mlchalek was a major study contributor from 1978 to 
1984 and has been a principal investigator since, while I have served as 
principal investigator since 1978. 

a. Reference your paragraph 1. Verification of all reported birth 
defects -in the. children fathej^ed by the participants in our study was con- 
ducted using medical records and birth certificates in 1984. Sixty one 
percent -of the defects reported by the Ranch Handers and their wives and 63X 
of. those reported by the comparisons were verified as being codable defects. 
These percentages were not statistically different, and there is no evidence 
of differential reporting of these data. The Ranch Hand children had in- 
creased numbers of birth defects, but the increase was in those children born 
to mothers who smoked during pregnancy. There was no evidence of any associa- 
tion with herbl c Ide expos ure b ut such a n as55P4lJ^ASIU^M3la>!-^^^''-'*->^'^-*Jt®>-"- 



\^r.<^ been ruled out. ^K^^eppT ag^^g^B^^yseiga^^^S^^^ 

^ j.^']^ \jjiX-The verincation of all reported birth defects'^has-resoTveT one smirce 6f~ 



\,^^ 



-%' 



possible bias in the study of reproductive endpoints (overreporting). 
ever, potential bias from underreporting remains. The negative reports on 
the remaining 5,614 children are currently being verified by medical record 
review. This is a very time-consuming process due to difficulties in locat- 
ing and obtaining records. Many of these "children" are now adults and their 
consent must be obtained before records can be requested. .1 anticipate 
completion of this effort by November 1988. The 'verified data will then be 
analyzed and the results will be released after review by the Advisory Com- 
mittee appointed by the Agent Orange Horkinj Group. 

b. Reference your paragraph 2. A series of flight tests was performed 
In C-123 aircraft In 1981 by Major Stephen L. Meek as background for a mas- 
ter's degree thesis at the University of Washington School of Public Health. 
The results of his work were considered in the development of the exposure 
assessments used in our data analyses. Unfortunately, technical difficulties 
were encountered In the conduct of the study, and the data were not as help- 
ful Mn clarifying exposure as we all had hoped. Further preliminary work was 
conducted by the Air Force Occupational and Environmental Health Laboratory 
to assess the feasibility of using glycerin as a simulant. However, full- 
scale simulations were not conducted due to operational difficulties. Addi- 
tionally, significant difficulties were encountered In developing scenarios 

^CO \>' h 

. '^ ^ 



83-529 95-4 



that accurately reflect the actual in-fUght conditions prevailing during the 
9 years the combat nissions were flown. The recent developwnt of a tech- 
nique to determine dioxin levels in serum will provide a direct measure of 
individual expssure without reliance on the assumptions and uncertainties 
implicit in simulation studies. 

^- ;••^ c._ Reference your paragraph 3. In May 1984, Or Bernadlne Bulkley (fdr- 
j:*^^ V'' ' Tmejrlyypf>Jhe»0ff1ce;of-; Science and Technology Pol1cy)»asked that we__yerj/y.r 
aJ-^ : ; several-of Tthe^selJnejTeport.'jre'sul tsT'^Howevejri^se^frVf 1«W^^ 
•^t,\^\ I, alrea3yt5nj3er>layj^yjpurfmff5pH^^^ occurred with 

C^C^. j,< the staff of the Office" of Scienc'e'i'nd Technology Policy in October 1986 to 
o'^ N^jJ^ provide them with an update of the Air Force study. No technical direction 
• ^\* was received at that time. They have acted as advocates of the program to 

obtain legislative support. The Air Force Surgeon General's office and the 
Air Force Systems Command (AFSC) headquarters have had no control over the 
science of the study. AFSC and Intervening staff offices have managed fund- 
ing and personnel resources, relieving the program scientists of these bur- 
densome but Important administrative tasks. 




editorial changes in writing style and emphasis , ^ ^„: .^^ 
were indicated. They felt the Executive ' r v-'" 
t'" Sumnary should be expanded, emphasis should be placed on an explanation of t^ . \ 

'^^i;^ elements used in determining causality, and other minor "wordsmi thing" f*^ 

??*■ changes should be made. The comments of the committee were Included in the * ■■ 

V final report. The initial morbidity report contained "followup" analyses of 

data which, unfortunately, are subject to misinterpretation. This difficulty 
has been mitigated in thi second morbidity report by strict adherence to a , 

preset statistical protocol. Specifically, while the Increment in Ranch Hand ^^7-. 
cancer appears limited to the skin, a systemic increase cannot be unambigu- _ 
ously ruled out. Similarly, the Increased reported birth defect rate may not |>:^ 
be confined to minor lesions. — '.' 

e. Reference your paragraph 5. All Interactions with the Advisory 
Committee have been purely technical in nature, idling exclusively with 
epidemiologic and statistical issues. The concerns of veterans were foremost 

.41-Y ., in the initial decisions in 1978 and 1979 to proceed with.,th1s^tudy.,;^43iy, 
'•^ 11 tJipgiBhj^^^iSjeanslVgroupirepresentatlve'was^ot on-the coiiroitteeV^^^^ 

cbncernsTare^addressed'.'^. We are committed to caring for the Air Force commu- 
^ . r^^^' nity, including retired and separated Air Force veterans. Their welfare is 
v^ our first priority. 

f. Reference your paragraph 6. The Australian, Centers for Disease 
Control (COO, and Air Force studies are relatively consistent in their 
conclusions. However, while they do not assert a causal relationship between 
Agent Orange and adverse health, a clear exoneration of the defoliant and its 
dioxin contaminant is not supported. All of these studies, Including the Air 
Force-sponsored research, suffer from some limitations. The studies have 
been limited in their ability to accurately measure individual levels of 
exposure to the chemicals, and a more precise estimation of exposure is 






95 



needed before definitive conclusions can be made. The COC birth defect and 
Air Force studies are the only ones specifically addressing Agent Orange with 
dioxin exposure. The others are limited to the effects of Vietnam service, 
and the findings cannot be interpreted as the result of Agent Orange. All of 
these studies suffer from misclassification of exposure. The opportunity to 
make more accurate exposure assessments in our study is available with the 
serum dioxin assay. Design problems in the COC and the Australian birth 
defect studies were apparent in their inability to control for the pre-Yiet- 
nara reproductive experience of the study groups. Similarly, the lack of 
medical verification of the birth certificate data is a significant weakness 
in these studies. Due to the small number of deaths occurring to date in 
these relatively young populations, all of the mortality studies suffer from 
low statistical power to detect increases in important disease categories. 
Despite their limitations, these six studies have been conducted as carefully 
and as scientifically as possible, and they have made major contributions 
toward the clarification of the Agent Orange/dioxin controversy. 

g. Reference your paragraph 7. The weight of scientific evidence from 
'epidemiologic studies in humans does not confirm a 1 ijk between A gent Orange 
arid adverse health n or doe s it rule out such a link. ^ 5or)fgiTi'>ietli|^jtgVjfni4W£y g? 
lI?aeT^K11S1v?nfdTgStefls S Latency periods for malignan't" disease a"re just " 
being reached, and studfes have identified several findings which need to be 
reevaluated in subsequent examinations to determine their clinical relevance.- 
At this time. Agent Orange cannot be implicated or exonerated. 

h. Reference your paragraph 8. Additional work in establishing' exposure 
through the use of the serum dioxin assay is needed. This assay xil} reduce 
uncertainties in estimating individual exposures and will significantly 
decrease any misclassification in the analysis of the data from the Air Force 
study. We are currently working with the COC to Implement this procedure for 
the analysis of the 1987 physical examination data. This procedure will 
Improve our exposure assessments and should support more solid statistical 
and epidemiologic conclusions if it is applied to al_l_ participants, including 
the comparisons. In the context of the Air Force study, the dioxin assay 
presents a unique opportunity to clarify the dioxin issue. 

i. Reference paragraph 9. The principal investigators In the Epidemi- 
ology Division have full and final responsibility for the science of the 
study. The Advisory Committee has scientific .oversight of the study and 
works closely with_the Air Force team. The Air Force management structure 
-^ j^limits its Impact on the study to purely. adm1n\strativejnatters of_ funding, 
]i-^i manpower and equipment management. ^hOrtbber 1984; .the^tonSandef "of_the ;■■* 
I* 'lJSAfrSchoolIof.''AeYds"parce'Medicine'riesolved an'lBpasseJ.ajion'gl^^ * 

lV 1nvest1gatbrs"concern'ingrth€ f'orina't of the"^1984 "Mortality Report. "It was' •> 
>,-v 1a't?r"very"c1ear'-that'J)1srsolut1on -was scientifically correct.' 'All reports 
^' are released by the A1r Force Surgeon General In the form approved by the 

Advisory Committee. The report of the 1985 physical examinations is cur- 
rently being prepared for review by the Advisory Committee, and public re- 
lease is expected in the fall of this year. Similarly, the 1987 update of 
the ongoing mortality study is expected in January or February 1908. 



/. 



96 



j. Reference your parigraph 10. The principal Investigators have at- 
V tended scientific neetings In this and other countries to freely exchange 
^ ,. \ Information on the Agent Orange/dioxin issue. .Telephone and mail contacts 
"■"vlrare equally unrestricted. For a tine after the release of the first nnrbid- 
">!! ity.>eport.5;iV^ebruary .U84.;an.publ1cjnqujr1esj(^^ through - 

S^ ' the^MbVfc^Vf fairs 'Office: all questions iSBretasSereaTby.'deslgn'atedMndl-a* 
' ' vTdiSj?- 

I hope this material Is of assistance to you and your staff. 
Sincerely 



Mi/^ 



WILLIAM H. WOLFE-/Colonel. USAF, MC 
Chief, Epidein1;^gy Division 




97 




DEPARTMENTT OF THE AIR F(ycE 
USAF SCHOOL OF AEROSPACE MEOICK^ (AFS( 
BROOKS AIR FORCE BASE. TEXAS 7 




RECEIVED wuv 3 lyb"/ 



2 3 NOV 1987 



Ms Laura Petrou , . . . 

Aide to SenatorvThomas Daschle^, ' 

United States. Senate i.-. It.. .. • - 

Washington DC ^20510-0001 --/=.>;: ■ .- . ^ 

Dear Ms Petrou ., . ^,..^.' , 

In your telephone call to me "-on 2 November, you requested a copy of the draft 
of the 1984 Air, Force Health Study Morbidity Report and a copy of the statis- 
tical analysisrconducted on- the incomplete birth defect data. .., 

I was unablfr-to":Vocate.a'copyrof ;the draft Morbidity Report in my'files.-. 
After the-reviewi5of-thatdraft',by..'Dr Robert- Miller's, AdvisoryConuiittee, the . 
final versionofi;the-report was prepared and was only slightly changed from '' 



the draft,";^ Iihaveyocated:a',copy,of _thejcprnmjttee_ s reconmendations and 




late 1984, at the. urging of ;. the Air Force Surgeon General's Office. '"The " 
principal "investigators-.an'djthetAdvisory-Comniittee had major reservations^ .. 
about the validity of .that. analysis, since only 67S of the children -reported ■• 
to have birth-defects and hone of the 5,635 of those reported to be normal 
had been checked against medical records. The lack of verification of the 
health status of .these children made this 1984 analysis invalid. The report 
was prepared as an internal 'working document solely for the study investiga- 
tors and Dr Miller's Advisory Committee. Since the data were incomplete, any 
conclusions based, oa. that analysis are invalid and would be misleading. 

.The process'ofrobtaining the medical records and verifying the health status... 
of the remain1ng^children■:fathered by study participants. is proceeding on. 
schedule.- .^-.TheTanajysis.-'ofa^thaVdata .is planned for late 1 988 ."j- When that ^:-^'- 
analysis'.isYcotripleted,\a.report^'will" be, prepared, reviewed by the Advisory'-'- ;.;, 
Committee,'.,and. released to the public. -I will ensure that you receive a copy 
of ,that^!-epontr>';-'.^: -- ';■':-.", :^-■ .^ . ~ . '.'. • ' ■.'"'.'.'■" 

If -you, have-any -further-questions or need "more information on this matter, 

;.please.fcontact;Ms4Patrici,aVTurner,~,the. Assistant. for Congressional and Public 

^ (Af f a i r's^instheiPf f i ce'rof^^theTAi r^,- Force'iSurgeon'; Genera 1 ; ( commercial "tel ephone ' 



, , ., , _. ice:of*.the-}Air-Force!Surgeon: Genera 



Unittfl States ^a^T^Tl^^^ 



The Honorable Edward C. Aldridge, Jr. 
Secretary of the Air Force 
The Pentagon 
Washington, DC 20330 

Dear Mr. Secretary: 

I am writing to request 1) a copy of the 1984 Air Force Health 
Study's Draft Morbidity Report, which was prepared by the principal 
investigators of the Air Force's Ranch Hand study and presented to 
the Ranch Hand Advisory Coranittee, and 2) a copy of "the analysis of 
the partially verified birth defect data. . .carried out in late 1984" 
(see attached copies of Col. William H. Wolfe's letters to my 
office along with my July 2, 1987, letter initiating this request). 

Whig'tf^iCT^gre^Wg^^n g^ 

SecgEei^a ^iS^=^ a'^^'^*^*>^<^*"^^y"-*P^«^^'°"^"^'^ 

securS^^eaJfhSWaaigan^sgttigBeqHaSiT^orcegp'e^^ ir* 

unsaSSplSil!E^SEv*oin.'a5S?^i<:T:SV6Vrec^ 

Thank you for your attention to this 'very important matter. 
With best wishes, I am 

Sincerely, 



Tom Daschle 

United States Senate 



TAD/lp 
Enclosures 



99 




"mOf^ 



(a<^h(je 



USAFSAM-TR-88-3 



UNITED STATES AIR FORCE PERSONNEL AND 
EXPOSURE TO HERBICIDE ORANGE 



Richard A. Albanese. M.O. 



February 1988 



Interim Report for Period March 1984 - February 1988 

I Approved for public release; distribution Is unlimited. | 



USAF SCHOOL OF AEROSPACE MEDICINE 
Human Systems Division (AFSC) 
Brooks Air Force Base, TX 78235-5301 




'^^^ 



100 



NOTICES 

This Interim report was submitted by personnel of the Radiation Analysis 
Branch, Radiation Sciences. Division, USAF School of Aerospace Medicine. Human 
Systems Division, AFSC, Brooks Air Force Base, Texas, under Job order 
SUPTXXRH. 

When Government drawings, specifications, or other data are used for any 
purpose other than In connection with a definitely Government-related procure- 
ment, the United States Government Incurs no responsibility or any obligation 
whatsoever. The fact that the Government may have formulated or In any way 
supplied the said drawings, specifications, or other data, is not to be 
regarded by Implication, or otherwise in any manner construed, as licensing 
the holder, or any other person or corporation; or as conveying any rights or 
permission to manufacture, use, or sell any patented invention that may in any 
way be related thereto. 

The Office of Public Affairs has reviewed this report, and It is releas- 
able to the National Technical Information Service, where It will be available 
to the general public, including foreign nationals. 

This report has been reviewed and is approved for publication. 

RICHARD A. ALBANESE, M.D. /»OHN C. MITCHELL, B.S. 

Project Scientist ''Chief, Radiation Sciences Division 



JEFBJig^G. DAVIS, Colonel, USAF. MC 



101 



l»si 



riQN or THIS >*ct 



REPORT DOCUMENTATION PAGE 



KfSTIIICnVE MAOKINCS 



2*. SICUHITY CLASSIf ICATION AUTHOWTY 

]b. OfClAJSIFHUTION/OOWNOIUOINa SCMCOUU 



1. OlSTRItunON/AVAILMIUTY Of UPOKT 

Approved for public release; distribution Is 
unlimited. 



4. nUraHMINC ORGANIZATION Rf PORT NUMICI«S) 
USAFSAM-TR-88-3 



. MONITORING 0R0ANI2ATION REPORT NUM1(R(S) 



te. NAMI or PERTORMING ORGANIZATION 

USAF School of Aerospace 
Medicine 



7«. NAME OP MONITORING ORGANIZATION 



USAFSAM/RZM 



c AOORESS (Cty, Sttn. »nt ZmCoUt) 

Human Systems Division (AFSC) 

Brooks Air Force Base, TX 78235-5301 



7b. AOORESS (C(y, sun. 



t. NAME OP PUNOING /SPONSORING 

USAF School Of Aerospac 



lb OPPICE SVMtOI. 



9 PROCUREMENT INSTRUMENT lOENTIPICATION I 



vfiflFSftn^'ni;n 



Cc. AOORESS rOiy. sun, tni ilfCodt) 

Human Systems Division (AFSC) 

Brooks Air Force Base, TX 78235-5301 



10. SOURa OP PUNOING NUMIERS 



ELEMENT NO 

65306F 



11. TTTU (Indudt Sanirrty CtenflulMn) 
United States Air Force Personnel and Exposure to Herbicide Orange 



I]. PERSONAt AUTHORS) 

Albanese, Richard A. 



W 



E^^OUNT 



t. SUMUMENTARY NOTATION 



II. SUIJEa TERMS (CanOniw on m«n* /' i 

Epidemiologic Investigation 
Phenoxy Herbicides 
Herbicide Orange 



Dloxln 

Ranch Hand 

Air Force Health Stud 



19. AISTRACT (Conttnu* en rtr»n» U nttttutf tnd i 
The United States Air Force Is conducting an epidemiological study, called the Air Force 
Health Study (AFHS), to determine whether or not military personnel associated with herbi- 
cide spraying during the Vietnam War have experienced any adverse health effects. This 
report reviews salient findings of the AFHS first morbidity report published In 1981, and 
presents new work by examining relationships between AFHS findings and the results of 
laboratory toxlcologlcal studies and other epidemiological studies addressing dloxln. 
Eleven clinical areas have been emphasized based on a toxlcologlcal profile developed from 
the literature and availability of data In the AFHS: weight loss, neoplasia, birth 
defects, neurological changes, psychological changes, hepatotoxlclty, chloracne, cardio- 
vascular changes, Immunological deficits, endocrine changes, and mortality. In six of 
these eleven clinical areas, statistically significant group differences occurred, and in 
five of these six Instances the group differences were In the direction of expected dloxln 



; RPT □ OTIC USERS 



00 Form 1473. JUN M 



SECURITY ClASSIPICATION QP TMIS PAGE 
UNCLASSIFIED 



102 



UNCUSSIFIEO 



19. ABSTRACT (Continued) 



effects. Oloxln cannot be confidently Identified as the causative agent of these findings 
!t this time because of several reasons. Including the absence of correlations with an 
e poSire ~ex !nd the incomplete clinical picture. However, dloxln '» "°' «;;°"«/^^f " 
a causative agent because of the directionality of the observed group dfferences and the 
preliminary nature of the exposure index used In the AFHS first »orbldlty report. 



$iC'J»>ITY CLASSIC 



103 



UNITED STATES AIR FORCE PERSONNEL AND EXPOSURE TO HERBICIDE ORANGE 
INTRODUCTION 



The United States Air Force is conducting an epidemiological study to 
determine whether or not military personnel associated with herbicide spraying 
during the Vietnam War have experienced any adverse health effects. The Air 
Force program responsible for the herbicide spraying was code named Operation 
Ranch Hand, and the personnel Involved in the spray missions are termed Ranch 
Hands. The current epidemiological study is called the Air Force Health 
Study (AFHS). 

This report reviews salient findings of the AFHS first morbidity report.^ 
Building on prior reports, this article presents new work by examining rela- 
tionships between AFHS findings and the results of laboratory toxlcologlcal 
studies anil other epidemiological studies addressing dioxln. This report 
attempts to assess the extent to which these initial AFHS findings are compat- 
ible with toxic effects of 2,3,7,8-tetrachlorodlbenzo para dioxln (TCDD) as 
known from animal experiments and, to a lesser extent, from observation In 
humans. In the preparation of this report, more than i»00 dioxin-related 
published articles were studied, and a biomedical portrait of dioxln effects 
emerged. This portrait will change as research proceeds; nevertheless, the 
current literature is sufficiently mature to permit comparison with AFHS 
findings. 



The Protocol 



Investigators at the USAF School of Aerospace Medicine developed a com- 
prehensive study protocol to govern the AFHS.^ The protocol underwent exten- 
sive peer review by military and civilian agencies, including: The University 
of Texas School of Public Health, an Air Force Scientific Advisory Board, the 
Armed Forces Epidemiological Board, the National Academy' of Sciences, and the 
White House appointed Agent Orange Working Group. This last organization 
continues to act in an advisory role. Recommendations by these groups were 
incorporated into the protocol. 



104 



study Design 

The study design is a matched cohort design in a nonconcurrent prospec- 
tive setting. The study addresses mortality and morbidity and Includes long- 
term follow-up activities. A detailed population ascertainment process iden- 
tified 1^278 Ranch Hand personnel who served in Vietnam during the period 1962 
through 1971, when the spraying operation was active. A comparison group was 
formed by identifying all individuals assigned to Air Force organizational 
units with a mission of flying cargo to, from, and in Vietnam during the same 
period. A computerized nearest neighbor selection process was used to match 
up to 10 comparison individuals to each Ranch Hand. This matching was done by 
Job category, race, and age. The initial comparison group erroneously con- 
tained some individuals who did not in fact have any Southeast Asia experi- 
ence. These individuals (18S) were removed from the comparison population 
after detailed hand record review, leaving an average of approximately eight 
comparison individuals matched to each Ranch Hand. 

The comparison individuals matched to each Ranch Hand were listed in 
random order within each set. The first five comparisons were included in the 
mortality analyses giving these studies a 1:5 design. For each living Ranch 
Hand, the first living member of his randomized comparison set was selected 
for participation in a morbidity study consisting of an in-home Interview and 
a comprehensive physical examination. If the matched comparison subject 
declined to participate or subsequently withdrew from the morbidity study, 
that individual was replaced by the next living comparison subject from the 
randomized set who was willing to participate. 

Follow-up studies are an important aspect of the AFHS. The follow-up 
studies consist of mortality and morbidity components. Each Ranch Hand and 
his set of comparisons will be the subject of mortality evaluations for the 
next 20 years. In addition, follow-up questionnaires and physical examina- 
tions are being offered to participants in 1985, 1987, 1992, 1997, and 2002 in 
order to bracket the latency periods associated with possible attributable 
disease. 



Inference Concerning Herbicide Causation 

In an experiment, members from a single population are randomly assigned 
to either a treatment (exposed) or control group. In the setting of such 
completely randomized designs, statistically significant differences between 
the treated and control group can often be reliably ascribed to the effect of 
the exposure. The AFHS Is the study of an unplanned environmental exposure 
and thus does not follow the above experimental design. The study has a non- 
randomized design and Is an observational study. In such studies, while the 
comparison group Is chosen to be similar to the exposed group with respect to 
as many qualities as possible, except exposure status. In the absence of 
randomization, group differences or the lack thereof cannot be Interpreted 
solely In terms of exposure. For example. In the AFHS the exposed group was 
stationed In the Republic of Vietnam Itself, while most of the comparison 



105 



group was quartered in surrounding areas such as Okinawa and Japan. Compari- 
son aircrew members periodically flew into Vietnam while comparison ground 
support personnel, predominantly enlisted, remained in non-combat areas. 
Ranch Hand Vietnam tour length was approximately 1 year while comparison tour 
length was 3 years. These differences and others may or may not influence 
health and longevity. Thus, group differences or the lack thereof cannot 
unambiguously be ascribed to herbicide exposure. This emphasizes the impor- 
tance of relating study results to other studies to see whether common pat- 
terns of effect emerge. 

Another approach to Inference is the use of an exposure measure or Index. 
If one knew exactly how much herbicide each Ranch Hand was exposed to, highly 
exposed individuals could be contrasted with less exposed Individuals within 
the Ranch Hand group and an estimate of herbicide effect could be constructed. 
However, once again, since randomization was not employed in the dose assign- 
ment, estimates of herbicide effect must be viewed with great care due to the 
possibility of confounding factors. For example, it could happen that higher 
exposures occurred for a variety of reasons in the lower socio-economic strata 
(lower ranks) of the Ranch Hand cohort. Industrial hygiene data concerning 
herbicide exposure were not collected during the Vietnam era. In any case, 
however, the use of an exposure index provides another view of exposure 
effects which can augment interpretation of group differences. 

The exposure index used in this report relates to the TCDD-contalnlng 
herbicides: Herbicide Orange, Herbicide Purple, Herbicide Pink, and Herbicide 
Green. Archived samples of Herbicide Purple had a mean TCDD concentration of 
approximately 33 ppm, and archived samples of Herbicide Orange had a mean 
concentration of 2 ppm. Herbicides Pink and Green contained twice the 2,'),5-T 
of Herbicide Purple and, therefore, have been estimated to contain TCDD at a 
concentration of approximately 66 ppm. 

Using mission records, it was possible to determine the amount of each 
herbicide sprayed each month in Vietnam as well as the number of Ranch Hands 
in each Job category who were Involved in spraying that month for the period 
1962 through 1971. Tour data also allowed determination of the months each 
individual was Involved in the Ranch Hand operation. Using these data, an 
exposure index was developed for each Ranch Hand. The exposure Index is 
directly proportional to the number of gallons of herbicide sprayed in Vietnam 
during the individual's tour, where potential exposure to the higher TCDD- 
contalnlng herbicides (Purple, Pink, Green) has been properly scaled according 
to dloxln concentration to place them on the same basis as Herbicide Orange. 
Also, the exposure index is inversely proportional to the number of airmen 
assigned to the specific subject's Job category during his tour. 

From the description Just given, it should be clear that the current 
Ranch Hand exposure Index is an estimate only, as it applies theater-wide 
spraying to a single individual, and, since it assumes that all individuals in 
a Job category were equally exposed. Also, the degree to which this calcu- 
lated index is associated with actual body burden of TCDD is unknown. In 
short, the absence of a positive association between the index and health 
outcomes cannot be taken as confirming a lack of herbicide effect, nor can the 
presence of an association be Interpreted as an unambiguous herbicide effect 
without consideration of possible confounding factors. 



106 



Job category matching In the AFHS used five categories: (a) officer- 
pilot, (b) officer-navigator, (c) officer-other, (d) enlisted-flying, and (e) 
enlisted-ground. Exposure index analyses used three occupational categories: 
all officers were combined into one category called "officer" due to the fact 
that navigators and pilots, while having different Jobs, were believed to be 
exposed in the same manner. For each exposure occupational group (officer, 
enlisted-flying, enlisted-ground), the calculated exposure index was trichot- 
onlzed into three levels: low exposure, medium exposure, and high exposure. 
Since the mode of exposure was Judged to be different in each occupational 
group, statistical analyses with the exposure index were occupational group 
specific. 



Questionnaire and Physical Examination 



The AFHS uses a broad medical history and physical examination. The 



medical history was collected by an extensive in-home questionnaire, 



The purpose of the extensive questionnaire was to collect data that could 
be analyzed for the subjective presence of adverse health effects that might 
be related to herbicide exposure. In addition to the study participants, the 
questionnaire contractor was also required to interview the participants' 
current and former wives, as well as the first-order next-of-kin of deceased 
individuals to obtain morbidity data as completely as possible. 

Physical examinations were performed at a single location by a contrac- 
tor. All examiners evaluated the participants without knowledge of their 
exposure status. The number of examiners and the turnover of staff members 
were kept to a minimum to limit between-examiner variability. All laboratory 
tests were subjected to rigid standards of quality control, and laboratory and 
physical examination data were measured on a continuous scale whenever possi- 
ble to improve statistical power in the analysis. 

A general summary of the major components of the examination is presented 
in Table 1 , and the laboratory procedures conducted on each subject are listed 
in Table 2. 



107 



TABLE 1 . AFHS PHYSICAL EXAMINATION 



General Physical Examination 

Neurological Examination 

Dermatological Examination 

Electrocardiogram 

Pulmonary Function Study 

Cheat X-ray 

Nerve Conduction Velocities 

Psychological Evaluation: 

Minnesota Multiphasic Personality Inventory (MMPI) 

Cornell 

Wechsler Memory Scale I 

Wechsler Adult Intelligence Scale (WAIS) 

Wide Range Achievement Test (WHAT) 

Halstead-Reitan Neuropsychological Battery 



108 



TABLE 2. LABORATORY PROCEDURES 



Chemistry Panel: 



Urinalysis: 



Blood Urea Nitrogen (BUN) 

Creatinine 

Cholesterol 

High-Density Lipoprotein 

Triglyceride 

Total Bilirubin 

Direct Bilirubin 

Alkaline Phosphosphatase 

Glucose (Fasting and 2 hour) 

Cortisol (Fasting and 2 hour) 

Serum Glutamic-Oxaloacetic 

Transaminase (SCOT) 
Serum Glutamic-Pyruvic 

Transaminase (SCPT) 
Gamma Glutamyl Transpeptidase 

(CGTP) 
Lactic Acid Dehydrogenase (LDH) 
Creatine Phosphoklnase (CPK) 
Blood Alcohol 



2'»-Hour Urine 
Volume 

Delta Amino Levullnlc Acid 
Coproporphyrlns 
Uroporphyrins 
Porphobilinogen 
Creatinine 

Semen Analysis: 

Volume 
Count 
Abnormal Forms 

Hepatitis B Testing: 

Surface Antigen 

Antibody to Surface Antigen 

Core Antibody 



Hormone Assay: 



Luteinizing Hormone (LH) 
Follicle Stimulating Hormone 
Testosterone 

Triiodothyronine (T3) Uptake 
Tetralodothyronlne (TU) 
Free Thyroxine Index (FTI) 



(FSH) 



Hematology Panel: 



Erythrocyte Sedimentation Rate 
Prothrombin Time 

Serological Test for Syphilis (RPR) 
White Blood Cell Count 

(with 10,000 cell differential) 
Red Blood Cell Count 
Hemoglobin 
Hematocrit 
Red Cell Indices 
Platelet Count 



109 



RESULTS 

Morbidity 

The results of the analysis of the baseline morbidity data were released 
In February 198'4j Of all Ranch Hand and comparison Individuals who were 
selected for the questionnaire and physical examination phases of this study, 
99. 5J were contacted, eliminating the major concern of selection bias. One 
thousand one hundred and seventy-four (97X) of the Ranch Hand group and 956 
(93?) of the originally selected comparison group participated in the ques- 
tionnaire portion of the Morbidity Study. An additional 576 comparison sub- 
jects were interviewed as substitute subjects, bringing the total number of 
comparison participants to 1,532. Substitute comparisons were selected to 
replace comparisons selected erroneously and to replace noncompllant compari- 
sons. Two thousand seven hundred eight current and former wives of the study 
participants were also Interviewed. One thousand and forty-five (87X) of the 
Ranch Hand group participated In the physical examination, and 773 (76$) of 
the originally selected comparison subjects participated in the examination 
process, giving a total of 2,269 participants. 

The analyses presented in the baseline morbidity report were largely 
performed using all available Ranch Hand data (1,0M5 participants) and data 
from originally selected comparison subjects (773 participants) yielding a 
total of 1,818 subjects. Data from the substitute comparison subjects were 
not used for inference. Due to logistic difficulties, the substitute compari- 
sons were invited to participate in the physical examination later in the 
study period; therefore the substitute comparisons had a narrower time window 
within which to travel to the examination site. The substitute comparison 
subjects, entered early into the study to replace Ineligible subjects, were 
found to be statistically comparable to the original comparisons when evalu- 
ated on clinical endpoints. Some principal investigators were concerned that 
the group substituting later for noncompllant comparisons may have self 
selected differently due to the reduced scheduling opportunity. Since opin- 
ions differed, a management decision was made to use only the originally 
invited comparisons for inference. 

The baseline morbidity report had 13 primary clinical chapters address- 
ing: general health, neoplasia, reproduction, neurological status, psycholog- 
ical status, hepatic function, dermatologlcal findings, cardiovascular 
conditions, immunological competence, hematopoietic status, and renal, pulmo- 
nary, and endocrine functions. More than 190 clinical variables were tabu- 
lated. In this report only a subset of these variables will be discussed. 
The variables selected for emphasis in this report were chosen because of the 
availability of corresponding or related evaluations In laboratory or other 
epidemiological studies related to dloxln effects. Thus, this report reflects 
on the degree to which AFHS findings are compatible with TCDD toxic effects as 
currently suggested by experiments with animals and observations in humans. 
Sample sizes may vary In adjusted analyses due to missing covarlate or end- 
point data. In all analyses, the phrase "statistically significant" refers to 
a p value of less than or equal to 0.05. 



110 



The fixed sample sizes In this study Impose limits on Its ability to 
detect small relative risks for rare diseases. This ability Is expressed In 
probabilistic terms using the statistical quantity called power, which Is 
defined as the probability of detecting a group difference of Interest. In 
the case of dlchotomous response, such as presence or absence of disease, 
groups are generally compared with relative risk, defined as the ratio of the 
probability of disease In the exposed group to the probability of disease In 
the comparison group. A relative risk of two, for example, would Indicate a 
doubling of the disease rate In the exposed group relative to the comparisons. 
If the disease Incidence In the control group Is 1/1000, as Is typical for 
some specific cancers, such as bladder cancer, the AFHS would require 22,8<tO 
exposed and an equal number of comparisons to attain a power of 80J to detect 
a relative risk of two, assuming two-sided testing with a 5i significance 
level. In fact, the AFHS Is unable to detect relative risks less than eight 
In diseases with a comparison Incidence of less than or equal to 1/1000. 
There Is a 0.351 chance of observing no cases at all of a rare disease of 
Incidence 1/1000 In a group of 1,0«5 subjects. With even rarer diseases of 
incidence, 1/10,000, there Is a 90% probability of observing no cases at all 
in a group of 1 .OMS subjects. 

This study does have good power to detect small relative risks for dis- 
eases having an incidence of 5/100 or greater. For example, the power for 
detecting a relative risk of 2, when the disease rate in the comparison popu- 
lation is 5/100, is 0.85, based on only 450 pairs in a matched pair analysis. 
In the case of continuously distributed response variables, such as blood 
pressure or cholesterol, this study has good power to detect small mean 
shifts. For example, the probability of detecting a mean shift of 5% in a 
matched pair analysis utilizing only 450 pairs is at least 0.90, assuming 
equal variances, two-sided testing and an 0.05 significance level. 

The power of the mortality component of this study is similarly con- 
strained. The mortality study design consists of all 1,247 Ranch Hands and up 
to 5 matched controls per Ranch Hand. The mortality study has a power of 0.85 
to detect a relative risk of two for causes of death, such as heart disease, 
having incidence 1/100 in the comparison population. The corresponding power 
Is less than 0.25 for causes having an incidence of 1/1000 in the control 
population. 

This study, in summary, has good power for detecting relative risks on 
the order of two or three for common diseases and causes of death and has 
virtually no power for detecting relative risks of the same order of magnitude 
for rare diseases. It does have good power for detecting small mean shifts in 
continuously distributed response variables. Bearing these study power con- 
straints in mind, the following ten areas of clinical morbidity are discussed. 

General Health 

Weight loss has been frequently reported as a consequence of subacute and 
chronic administration of TCDD to animals. McNulty^ noted marked weight loss 
in two male rhesus monkeys fed diets containing 2 or 20 ppb TCDD. Horses 
ingesting TCDD-contaminated waste oil sprayed on arenas in Missouri showed 
significant weight los3.''° Chapman and Schiller' report that decreased feed 
consumption did not account tor weight loss in C57 mice given dloxln in their 



Ill 



feed. Seefeld and colleagues" conclude that TCDD affects the weight regula- 
tion set-point In rats. Weight loss has not been prominently commented on in 
studies of human exposure. However, Oliver' indicates weight loss or loss of 
appetite In two of three reported cases. 

The toxlcological literature mentioned here suggests that weight changes 
might be anticipated In a dloxln-exposed group. In the AFHS, body fat percent 
was calculated by a formula that uses height and weight as Independent vari- 
ables.^" No statistically significant differences In the distribution of 
estimated body fat were detected between the Ranch Hand and comparison group. 
The basic data are shown In Table 3. 



TABLE 3. DISTRIBUTION OF BODY FAT PERCENT 

Lean (<10t) Normal (10-25J) Obese 025J) 

Number Percent Number Percent Number Percent Total 

Ranch Hand 13 (D 82U (79) 207 (20) 1 .OHM 

Comparison 7 (1) 607 (79) 157 (20) 771 



The sample sizes In Table 3 (I.OUt and 771) are reduced due to missing 
data for three Individuals. A chi-square statistical test using these data 
indicated no statistically significant difference between the distributions 
for the groups (p-0.89). Detailed analyses of percent body fat, adjusting for 
age, race, and occupational category, are described In the baseline report, 
and these analyses also indicated the absence of a group difference. Also, 
within the Ranch Hand group no relationship between body fat and the exposure 
index was found. 



Neoplasia 

The animal toxicology literature portrays dloxln as a carclnoaen, a 
cocarclnogen, and as having antl-carclnogenlc properties. Jackson showed 
Impairment In the functioning of the mitotic apparatus at 0.2 ug/1 In dividing 
endosperm cells of the African blood Illy. Koclba et al^^ fed male and female 
Sprague-Dawley rats on diets supplying 0.1, 0.01, or 0.001 ug of TCDD/kg/day 
for 2 years. Exposed male rats displayed more stratified squamous cell carci- 
nomas of the hard palate and tongue. However, fewer adenomas of the pancreas 
and pheochromocytomas of the adrenal were found. Kouri and colleagues 
conclude that TCDD is a cocarclnogen. They propose that this effect Is medi- 
ated through aryl hydrocarbon hydroxylase Induction. On the other hand, 
DlGlovannl and colleagues^ found that TCDD reduced cutaneous papilloma forma- 
tion by various hydrocarbons. Indicating an antl-carclnogenlc effect. With 
respect to carcinogenesis In man, Coggon and Acheson'' reviewed the available 



112 



epidemiological studies and concluded "... there is suggestive evidence of a 
biological association between phenoxy herbicides (or their contaminants) and 
soft-tissue sarcomas. The. evidence relating these products to the occurrence 
of lymphomas is weaker." 

Table U summarizes the cancer events that have occurred in the Ranch Hand 
and comparison groups since these Individuals completed their Southeast Asia 
military tours. All shown cancer cases have been verified by personal medical 
or pathological records. One comparison individual has had both a skin and 
systemic cancer. In the table below he is shown as having only a systemic 
cancer for purposes of the statistical analysis. 



CANCER VERIFIED BY INDIVIDUAL MEDICAL RECORDS OR PATHOLOGY REPORTS 



Croup 


No. with 
Skin Cancer (J) 


No. with 
Systemic Cancer (<) 


No. with 
No Cancer (J) 


Total 


Ranch Hand 
Comparison 


35 (3.3) 
10 (1.3) 


13 (1.2) 
8 (1.0) 


997 (95.'*) 
755 (97.7) 


1,0U5 
773 



Of 1 .CJS Ranch Hands, U.59i have a skin or systemic cancer. Of the 773 
comparison individuals, 2.33J have a skin or systemic cancer. Thus, the 
relative risk for any type of cancer is 1.97 and this relative risk has a 
probability of less than 0.01 of occurring by chance under the hypothesis of 
no difference. This statistical test for overall cancer rate difference was 
the hypothesis test formulated prior to examination of the cancer data set. 
After this statistical test was performed, detailed review of the cancer data 
file suggested that the file be partitioned into skin and systemic events 
based upon the observation that skin cancer comprised a large fraction of the 
cancer set. The relative risk for skin cancer is 2.59, and this risk has a p 
value of less than 0.01. The relative risk for systemic cancer is 1.20, and 
this risk has a probability of 0.67 of occurring by chance. 

In the first morbidity report, the authors felt the neoplastic process 
was confined to skin. This inference cannot be affirmed because the separate 
skin and systemic hypothesis tests followed rather than preceded review of the 
cancer data file; thus the critical levels for these tests are unknown. 
Furthermore, important increments in relative risk for systemic cancer could 
be missed by chance mechanisms because of the small sample sizes in the AFHS. 
Neither skin cancer nor systemic cancer rates were correlated with herbicide 
exposure level; however, these statistical analyses Involved a very small 
number of cases in most of the nine occupation-exposure categories, thus 
decreasing the precision of rate determinations in these categories. 



113 



Reproduction 

The literature suggests that dloxln has mutagenic and teratogenic capac- 
ity. Some bacterial tests have been positive for TCDD mutagenicity. The 
baby hamster kidney cell transformation assay was positive for TCDD mutage- 
nicity. Chromosome aberrations have been seen in bone marrow cells of male 
rats exposed to TCDD.'' Van Miller and Allen ° observed reduced spermato- 
genesis in rats experiencing chronic exposure to TCDD. Seller ' observed 
reduced DNA synthesis in mouse testicle. Courtney and Moore^° observed kidney 
abnormalities in fetuses of female rats given 0.5 ug/kg/day of TCDD subcuta- 
neoualy on days 6-15 of gestation. Cleft palate and renal abnormalities have 
been produced in the mouse after oral or subcutaneous administration of TCDD 
to females. Lamb and colleagues^^ showed that exposure of male mice to 
toxic levels of TCDD with subsequent mating did not affect sperm, mating 
frequency, or quality of offspring. 

This sampling of the literature should be sufficient to indicate the 
possibility of reproductive changes in exposed human populations. Hanify and 
colleagues^^ f,ave reported an association of aerial spraying of 2,1,5-T and an 
excess of talipes in New Zealand. Townsend et al.,^ in a study of Dow chemi- 
cal workers' wives, found no statistically significant differences in fetal 
wastage or t)irth defects. The Australian government's study of birth defects 
in Vietnam veterans showed no statistically significant differences in rates 
between veterans who served in Vietnam and those who did not." A Centers for 
Disease Control study (CDC) also found Vietnam veterans to have the same 
overall risk for fathering abnormal offspring as nonveterans. In the CDC 
study some specific defects were associated with higher exposures, but inter- 
pretation of this finding was uncertain.^ 

Male exposure could theoretically lead to unfavorable reproductive out- 
comes by means of several mechanisms: (a) mutated DNA In sperm, (b) abnormal 
sperm or testicular function due to biochemical effects, (c) transmission of 
TCDD to the female by spermatic fluid, and (d) transmission of TCDD to the 
female by contact with clothes or other objects. 



114 



Semen specimens from study participants without vasectomies or orchiec- 
tomies evidenced no statistically significant group differences in sperm count 
or percent abnormal sperm. The data are displayed in Table 5. Sample sizes 
reflect the number of compliant subjects not previously vasectomlzed. 

TABLE 5. DESCRIPTIVE STATISTICS OF SPERM VARIABLES BY GROUP 
Sperm Count (millions/ml) 



Ranch Hand (N-572) 111.5 102.8 
Comparison (N-1421 ) 111.9 108.8 



Percent Abnormal Sperm 



Ranch Hand (N-560) 9.7 5.5 

Comparison (N-409) 9.6 5.2 



115 



Conceptions reported by study participants and their spouses were catego- 
rized as miscarriages, stillbirths, Induced abortions, and live births. Num- 
bers In each category are shown In Table 6 with Indication of whether the 
conception occurred before or following the participant's Southeast Asia tour. 



TABLE 6. CONCEPTION OUTCOMES BY GROUP MEMBERSHIP AND TIME 







Pre-SEA 






Post-SEA 








Yes 


(J) 


No 


Yes 


(J) 


No 


PJ^alue 


Miscarriages 
















Ranch Hand 


239 


(13.7) 


1.505 


156 


(15.0) 


883 


0.76 


Comparison 


172 


(11.9) 


1.276 


10U 


(12.5) 


726 




Stillbirths 
















Ranch Hand 


9 


(0.5) 


1.735 


12 


(1.2) 


1,027 


1 .00 


Comparison 


8 


(0.6) 


1,1440 


8 


(1.0) 


822 




Induced Abortions 














Ranch Hand 


8 


(0.5) 


1.736 


37 


(3.6) 


1,002 


0.89 


Comparison 


7 


(0.5) 


l.Uill 


33 


(«.0) 


797 




Live Births 
















Ranch Hand 


1,187 


(85.3) 


257 


833 


(80.2) 


206 


0.9K 


Comparison 


1,258 


(86.9) 


190 


682 


(82.2) 


1«8 





The data were analyzed using log-linear models^', adjusting for the fac- 
tors of maternal age (<35, ^35), maternal smoking (yes/no), maternal alcohol 
use (yes/no), and paternal age (<35, ^35). The four statistical tests all had 
p values greater than or equal to 0.76. Exposure analyses showed no consis- 
tent pattern with exposure level. 



116 



Ranch Hand and comparison live births were further analyzed to determine 
the occurrence of learning disabilities, physical handicaps, infant death, 
neonatal death, and birth defects. Data on live birth outcomes by group mem- 
bership and time are shown in Table 7. 



TABLE 7. LIVE BIRTH OUTCOMES St GROUP MEMBERSHIP AND TIME 





Yes 


Pre-SEA 
(J) 


Mo 


Yes 


Post-SEA 
(t) 


No 


P Value 


Learning Disability 










Ranch Hand 
Comparison 


57 
57 


(3.8) 
(H.5) 


1,430 
1.201 


75 
47 


(9.0) 
(6.9) 


758 
635 


0.19 


Physical Handicap 
















Ranch Hand 
Comparison 


134 
103 


(9.0) 
(8.2) 


1.353 
1,155 


126 
77 


(15.1) 
(11.3) 


707 
605 


0.45 


Infant Death 
















Ranch Hand 
Comparison 


7 

2 


(0.5) 
(0.2) 


1,480 
1,256 


3 


(0.4) 
(0.1) 


830 
681 


0.81 


Birth Defects 
















Ranch Hand 
Comparison 


78 
80 


(5.2) 
(6.4) 


1,409 
1.178 


76 
44 


(9.1) 
(6.5) 


757 
638 


0.04 


neonatal Death 
















Ranch Hand 
Comparison 


20 
17 


(1.3) 
(1.4) 


1,467 
1,241 


14 

3 


(1.7) 
(0.4) 


819 
679 


0.20 



Analyses of these data, adjusting for maternal age, maternal smoking, 
maternal alcohol use, and paternal age, reveals a statistically significant 
Increase in reported birth defects In the Ranch Hand group. Subsequent to 
this observation the birth defects were categorized as severe (life threaten- 
ing or interfering with normal overall health or socio-economic progress), 
moderate (not life threatening and, with health care, non-interfering with 
overall health or socio-economic progress), and limited (non-life threatening, 
non- interfering, and needing no care). These data are shown in Table 8. 



117 



TABLE 8. SEVERITY OF REPORTED BIRTH DEFECTS BY GROUP MEMBERSHIP AMD TIME 





Severe 

H (t) 


Pre-SEA 
Moderate Limited 
N (t) N (J) 


No reported 
Defects 


Total 




N (J) 




Ranch Hand 
Comparison 


51 (3.0) 
50 (3.5) 


32 (1.9) 7 (0.4) 
27 (1.9) 10 (0.7) 

Post-SEA 


1.633 (95) 
1,348 (94) 


1.723 
1.435 




N ($) 


N (J) N (i) 


N (S) 




Ranch Hand 
Comparison 


32 (3.5) 
18 (2.4) 


22 (2.4) 26 (2.8) 
20 (2.7) 10 (1.3) 


837 (91) 
696 (94) 


917 
744 



The above data set Is larger than the prior data set since this set 
contains all reported live births while the prior set consisted of all live 
births on whom the covarlates (maternal age, maternal smoking, maternal alco- 
hol, and paternal age) were available. The larger data set was used since 
categorizing birth defects as severe, moderate, or limited reduced cell 
counts. Full covarlate adjustment was not possible. The morbidity report can 
be consulted for details.' 

Once again. In this larger data set, an Increase In reported defects is 
noted. Specifically, the Ranch Hand to comparison birth defect odds ratio is 
0.85 for children born prior to Vietnam, while the post-Vietnam ratio is 1.39. 
A statistical analysis of the complete data set suggests that the birth defect 
severity pattern by group relationship changes with time (p-0.07). Visual 
inspection of these data suggests that this nearly significant change may be 
due to a relatively large number (26) of post-Vietnam Ranch Hand children 
reported as having limited birth defects; the Ranch Hand to comparison odds 
ratio in this category is 2.16. However, an excess of severe defects is also 
seen by visual Inspection. A separate analysis on data for defective children 
only (with the reported non-defective children removed) suggests that the 
group by severity relationship does not change with time (p-0.l5) and that the 
severity pattern does not change with group (p-0.78). The statistical analy- 
sis of the complete data set Is more powerful than these last two analyses 
since the latter analyses use only the 305 reportedly defective children, 
which constitutes only 6.3J of the total data set. 

In the AFHS first morbidity report, it was asserted that minor skin 
lesions accounted for the reported birth defects excess. That analysis was 
Incomplete, and we are no longer confident In that Inference. Also In the 
AFHS first morbidity report. It was properly suggested that differential 
reporting of birth defects could be responsible for the apparent excess. A 



118 



preliminary analysis of medical records of children reported abnormal, has 
indicated that overreportlng of defects may not account for the excess; how- 
ever, Intensive work is in progress addressing both differential over- and 
underreporting. 

Exposure index analysis of the birth defect data yields Inconsistent 
findings that are not interpretable as a herbicide effect. 

The finding of Increased birth defects as reported by study participants, 
their wives, and partners is under further investigation by review of birth 
certificates and medical records of all 5,663 children to verify both positive 
and negative responses. 

Neurological Findings 

A variety of neurological symptoms have been described following indus- 
trial accidents involving TCDD including headaches, asthenia, sleep distur- 
bances, irritability, and confusion. Peripheral polyneuropathy is a specific 
neurological condition that has also been linked to acute dloxln exposure, and 
is a condition that is amenable to direct clinical measurement. ^° Elovaara 
and colleagues^' found that acid proteinase activity was increased In the 
brains of Wlstar rats after TCDD treatment. Acid proteinase is a lysosomal 
enzyme responsible for protein destruction in the mammalian brain, and may 
play a role in degenerative diseases and intoxications. 

In the AFHS, neurological examination of the twelve cranial nerves 
revealed no statistically significant group differences. Assessment of 
peripheral nerve status included sensitivity to touch, vibration, and test of 
the patellar, achllles, and biceps reflexes. Again, no statistically signif- 
icant group differentials were observed. 

As shown in Table 9, the groups were not statistically different with 
respect to nerve conduction velocities. Of Interest is the observation (data 
not shown) that the conduction velocities decreased as expected with increas- 
ing self-reported alcohol use (drink-years) and postprandial glucose levels 
(dichotomized as less than, or equal to or greater than 120 mg/dl). These 
effects appear to be consistent in both groups. All exposure index analyses 
were unremarkable. 



119 



TABLE 9. MERVE CONDUCTION VELOCITY (M/SEC) 



Nerve 


Croup (N) 




Unadjusted 


Mean 


P Value 


Ulnar 
(above the elbow) 


Ranch Hand 
Comparison 


(1.035) 
(769) 


55.9 
56.2 




0.30 


Ulnar 
(below the elbow) 


Ranch Hand 
Comparison 


(1012) 
(771) 


60.5 
60.7 




0.39 




Ranch Hand 
Comparison 


(10141) 

(769) 


48.2 
U8.1 




0.7U 



Psychological Assessment 



30 



Working with rats, Creso et al.-'" have noted that TCDD provokes irrita- 
bility, aggressiveness, and restlessness. They found by in vitro studies that 
TCDD directly stimulates the striatal and hypothalamic adenylate cyclase of 
rat. Oliver' reports that two of three TCDD-exposed individuals studied 
expressed the symptom of excessive fatigue, and one communicated loss of 
ability to concentrate. Bauer et al.^^ studied nine workers with chloracne 
and noted fatigue and apathy alternating with anger and irritability. Rorshach 
tests showed a weakened emotional reaction, slowed thought processes, and 
perseveration. Poland and Smith'^ observed increased values on the MMPI mania 
scale in the group of workers with chloracne when compared to two groups with 
less severe acne. 

The AFHS disclosed several group differences in psychological testing. 
Indices developed from the questionnaire relating to fatigue, anger, mental 
erosion, anxiety, isolation, and depression all showed Ranch Hands to be sta- 
tistically significantly less well than comparisons. The Cornell index 
results paralleled the questionnaire indices; however, no increase in Ranch 
Hand depression was seen. Education strongly related to results of all psy- 
chological testing with group differences tending to be most prominent In 
high-school-only educated Individuals rather than college educated. For 
example, the MMPI among high-school-only educated individuals showed statisti- 
cally significantly higher hypochondria, mania, and social introversion scores 
among Ranch Hands. The MMPI among college-educated participants showed only 
higher social introversion among Ranch Hands. In Interpreting these data it 
must be remembered that there is a very high association between being college 
educated and having officer status. None of these data had been adjusted for 
the potentially confounding variable of combat stress. This area was pursued 
during the 1985 follow-up examination. Tests aiming at neuromuscular and 
Intellectual functioning (WAIS and Halsted-Reltan) showed no group differ- 
ences, and no consistent patterns emerged from any analyses using the exposure 
Index. 



120 



Thirty-six of 1 ,0i«5 Ranch Handera O-iit) and 16 of 773 comparisons (2.1 J) 
reported psychological illness (psychosis, alcohol dependence, anxiety, or 
other neurosis). This group difference is not statistically significant. 

Hepatic Examination 

Dioxin has been associated with the occurrence of hepatotoxicity. Pro- 
liferation of the smooth endoplasmic reticulum, distortion of liver architec- 
ture, and increase in liver weight relative to body weight have been seen in 
rats and mice. Changes in serum enzymes have been observed, but not with 
consistency. Porphyria has been observed after chronic dosing. A sampling of 
an extensive literature is given next. Weber et al.33 observed rats over a 
32-week period following a single intraperitoneal dose (20 ug/kg) of TCDD. 
Centrolobular necrosis, mitochondrial lesions, smooth endoplasmic reticulum 
increase, and hepatic regeneration were seen. The abnormalities began to 
regress 16 weeks after exposure. Similar findings in rats have also been 
reported by King and Roesler.^ Gupta and colleagues^' orally administered 
single, daily, and weekly doses of TCOO to rats, guinea pigs, and mice. Severe 
liver lesions were only seen in the rat indicating species variation. Kociba 
et al.'^ noted elevated liver enzyme levels in rats fed diets with TCDD for 
two years. Porphyria cutanea tarda has occurred in workers exposed to TCDD, 3° 
and porphyria has been observed in rats.^ 

Sweeney and colleagues^' have performed work that shows a synergism 
between the effects of TCDD and systemic iron. Iron deficiency was seen to 
prevent TCDD-induced porphyria in mice. In iron-deficient animals, TCDD was 
not able to decrease uridine decarboxylase levels. Iron deficiency protected 
mice against skin damage and the disruption of hepatic architecture seen with 
TCDD. Mixed function oxygenase activity was induced by TCDD in iron-deficient 
animals to a lesser degree than in non-deficient animals, but this difference 
was not significant. Sinclair and Granick" had earlier seen that iron was 
needed for uroporphyrin formation induced by chlorinated hydrocarbons. Smith 
et al.3' noted an increase in hepatic iron content 3 weeks after a 75 ug/kg 
oral dose of TCDD to C57BL/10 and DBA/2 mice. Increased intestinal uptake of 
iron has been observed in mice and rats after TCDD exposure." 

In the AFHS, nine biochemical determinations of liver function were made: 
SCOT. SCPT, GGTP, alkaline phosphatase (Alk.Phos.), total bilirubin (T.Blli), 
direct bilirubin (D.Bill), lactic acid dehydrogenase (LDH), cholesterol 
(Choi), and triglycerides (Trig). In the analyses of these nine variables, 
statistical adjustments were made for four covariates: current alcohol inges- 
tion (self-reported in drinks per day), self-reported days of exposure to non- 
herbicide industrial chemicals, self-reported days of exposure to degreaslng 
chemicals, and presence or absence of antibody to hepatitis B surface antigen 
(anti-HBsAg). 

Table 10 provides unadjusted and adjusted means and percent abnormality 
by group for the nine hepatic-related variables. The standard age-adjusted 
criteria for abnormal laboratory values were used throughout. No obvious 
group differences are apparent in these data. However, the statistical 
modeling of the dependent variables with the covarlables showed three group 
differences. The Ranch Hand SCOT-alcohol regression slope is 0.0178 base-lO 
logarithmic units per drink per day while the comparison slope Is 0.0113. 

18 



121 



These slopes mean that among study participants who report one drink per day, 
Ranch Hand SCOT levels are 1.5< higher than comparison levels. Among study 
participants who had four drinks per day, Ranch Hands have SCOT levels 6.81 
higher than comparisons. 



TABLE 10. 


UNADJUSTED MEANS, ADJUSTED MEANS, 
FOR NINE LIVER-RELATED VARIABLES 


, AND PERCENT 


ABNORMALITY 


Variable 


Croup 




Unadjusted 
Means 


Adjusted 
Means 


PCT Outside of 
Normal Range 


SCOT 


RH« 
Com»» 




33.0 
33.1 




33.0 
33.1 




13.9 
14.8 


SGPT 


RH 

Com 




20.3 
20.5 




20.3 
20.5 




7.8 
8.6 


COPT 


RH 
Com 




HO. 2 
39.3 




40.1 
39.3 




10.8 
10.3 


Alk.Phos. 


RH 
Com 




7.68 
7.53 




7.69 
7.52 




17.3 
16.9 


T. Bill 


RH 
Com 




0.57 
0.58 




0.57 
0.58 




1.8 
2.0 


D. BUI 


RH 
Com 




0.23 
0.2U 




0.23 
0.2U 




29.0 
29.7 


LDH 


RH 

Com 




1112.1 
1U1.7 




1142.1 
141.7 




1.7 
2.1 


Choi 


RH 
Con 




212.2 
216.6 




212.2 
216.6 




26.0 
27.7 


Trig 


RH 

Com 




121.8 
12i».3 




121.9 
124.1 




34.7 
36.1 



•RH denotes Ranch Hand 
••Com denotes original fully compliant comparisons. 



LDH-alcohol slopes were 0.0041 logarithmic units per drink per day In the 
Ranch Hand cohort and -0.0008 in the comparison group (p-0.011). The LDH- 
degreasing chemical slopes were 0.000005 and -0.0000008 logarithmic units per 
day degreasing chemical exposure in the Ranch Hand and comparison groups 
respectively (p-0.037). 



19 



122 



RH 
Com 


30.5 
30.8 


RH 

Com 


31.2 
30.8 


RH 
Com 


2328.9 
2383.2 



Twenty-four-hour urine collections were obtained for 620 Ranch Hands and 
'•39 comparisons; uroporphyrins, coproporphyrlns, and d-aminolevullnic acid 
were determined. Unadjusted group means are shown in Table 11. 



TABLE 1 1 . UNADJUSTED GROUP MEANS FOR THREE COMPOUNDS RELATED TO PORPHYRIN 
METABOLISM 



Uroporphyrin 
Coproporphyrin 
d-aminolevulinic acid 



No statistically significant differences are obvious in these data. 
Detailed statistical analyses were done, simultaneously adjusting for six 
covariates: current alcohol use, blood urinary nitrogen, creatinine clear- 
ance, days of exposure to industrial chemicals, days of exposure to degreasing 
chemicals, and presence/absence of' antibody to hepatitis B surface antigen. A 
generalized linear model analysis was done for each of the three compounds 
with all six covariates examined simultaneously. The coproporphyrin-alcohol 
slope was *0.013 logarithmic units per drink per day in the Ranch Hand group 
and -0.008 logarithmic units per drink per day in the comparison group 
(p-O.OHS). No other group differences were statistically significant. The 
clinical relevance of these differences in slope is unclear. 

Sixteen of 1,027 Ranch Handers (1.56$) were diagnosed as having hepato- 
megaly at physical examination while six of 769 comparisons (0.78>) had that 
finding (p-0.138). Thirteen of 1,032 Ranch Handers had a verified medical 
history of liver disorder other than hepatitis. Jaundice, or cirrhosis veri- 
fied by medical record while two of 773 comparisons had the same (p-0.00'»). 

Throughout the hepatic analyses no variable showed a meaningful relation- 
ship with the herbicide exposure index. In all the above analyses no adjust- 
ments for iron metabolism were made. 



Dermatological Finding 

TCDD is known to cause chloracne. Chloracne is an acneiform lesion which 
tends to predominate in the areas of the face around the eyes, temples, and 
ears. Chloracne has been frequently seen in humans who have contacted TCDD in 
the context of industrial accidents. In one study the chloracne resolved 
within 1 year for the most part with no scarring. ' Chloracne has been noted 



123 



by many Investigators years after exposure and Is generally recognized as a 
persistent effect of dloxin exposure. Bovey and Young ^ conclude that "the 
presence of active chloracne months to years after exposure does not neces- 
sarily mean continuing exposure." 

In the AFHS, no active chloracne was found in either the exposed or com- 
parison group by examination or review of medical records. Also, as Indicated 
in Table 12, there were no statistically significant group differences with 
respect to chloracne-related lesions. No statistically significant regres- 
sion trends were noted with the exposure index. 



TABLE 12. PREVALENCE OF DERMATOLOGIC DIAGNOSES IN PERCENT 





Ranch Hand 


Comparison 




Relative 


95 » 




N - 1045 


N - 773 


P Value 


Risk 


Conf Int 


Comedones 


21.7 


20.7 


0.60 


1.05 


(.87.1.26) 


Acneiform lesions 


18.3 


17.5 


0.66 


1.05 


(.85.1.29) 


Acnelform scars 


11.2 


10. J4 


0.57 


1.08 


(.82.1.43) 


Cysts 


11.6 


10.5 


0.U6 


1.10 


(.84,1.46) 


Hyperpigmentation 


8.3 


7.1 


0.35 


1.17 


(.84,1.65) 


Other abnormalities 12.6 


16.3 


0.03 


.77 


(.81, .98) 


Any abnormalities 


U5.0 


HU.9 


0.97 


1.00 


(.90,1.11) 



Cardiovascular System 

TCDD causes a rapid, dose-dependent elevation of llpofuscln In the hearts 
of female Fischer 344 rats. The authors of the research suggest that TCDD 
toxicity may be associated with radical- Induced lipid peroxidation. ^ Kociba 
and colleagues' 2 saw an increased incidence of arteritis in rats. In 1958, 
Schmittle and colleagues reported hydropericardium in poultry following 
ingestion of feeds contaminated with Industrial chemicals. In 1969 a dloxin 
was shown to be the hydropericardiuffl-producing factor in poultry. ^ Jlrasek 
and colleagues^" report that a 57-year-old male with chloracne developed 
unusually severe atherosclerosis and subsequently died. Moses and colleagues 
found that 17 of 116 workers with chloracne reported myocardial infarction 
(14. 7J) while 7 of 85 (8.2J) without chloracne reported the same (p > 0.10). 
Zack and Suskind^^ observed no excess in circulatory system 'deaths comparing 
events In Monsanto Company workers to standard US population rates. 

In the AFHS no statistically significant group differences were observed 
with respect to measurements of systolic and diastolic blood pressures. Also, 
the groups were not statistically significantly different with respect to 
numbers of abnormal electrocardiograms. Abnormal funduscoplc findings were 
not associated with group membership nor was the occurrence of carotid bruits. 
During the physical examination, 10 peripheral pulses were examined: the 
radial, femoral, popliteal, dorsalls pedis, and posterior tibial pulses. One 



124 



or more pulses in this set of pulses were found to be abnormal In 12. 8J (106/ 
829) of the non-black Ranch Hands, while 9.'*!l (56/596) were found abnormal in 
the comparison group (p«0.05). The group difference was not statistically 
significant in the data set on Black study participants, but this may only 
reflect smaller numbers. Peripheral pulse abnormalities tended to aggregate 
in older individuals (5 KO years) who smoked (> 10 pack years). The partici- 
pants were allowed to smoke prior to the examination of the pulses, and more 
Ranch Hands smoked at the time of the examination than did comparisons (K5.7X 
versus 40.5$, p-0.03). 

Data on the numbers of individuals in the Ranch Hand and the comparison 
group who had experienced some form of heart disease (ICD-9th edition, CM) or 
who had experienced a myocardial infarction are shown in Table 13. The num- 
bers shown are supported by medical record verification of participants' self- 
reporting. These data do not suggest a difference in ischemic heart disease 
in the two groups. 



TABLE 13. HEART DISEASE AND HEART ATTACK IN THE AFHS 



Ranch Hand Comparison 

Yes No Yes No P Value 

Verified Heart Disease 117 898 109 eeu 0.982 

Verified Heart Attack 7 1,038 3 770 0.H32 



Immunological Effects 

Clark and colleag 

vation in all animal species following TCDD exposure. They also observed 
reduced delayed hypersensitivity reactions assessed by ear swelling following 
oxazalone sensitization in 6- to 8-week-old mice. Cytotoxic T cell lymphocyte 
generation was impaired by low doses (O.OOt ug/kg) of TCDD. Following a 
variety of experiments, the authors suggest that TCDD may acutely decrease 
cytotoxic T lymphocyte generation by promoting the generation of suppressor T 
cells. In parallel results, Montovanl and colleages^^ observed decreased 
numbers of peritoneal macrophages and splenocytes in TCDD-treated 6- to 
8-week-old mice, while cytotoxic capability per unit number of cells was not 
affected. Van Logten and colleagues^ conclude that the atrophy of the thymus 
observed following TCDD administration in rats is not mediated by the adrenal 
or pituitary glands. Clark and colleagues^^ state that the Immunotoxic 
effects of TCDD in C57B/6 and DBA/2 mice occur at dose levels below those 
needed to induce hepatic mixed function-oxidase enzymes. 

In the AFHS, immunological status was assessed in 592 participants by (1) 
the enumeration of T-lymphocytes, T-lymphocyte subsets, and B-lymphocytes 
using monoclonal surface marker analysis, and by (2) the assessment of 
lymphocyte ability to respond to selected antigen or mitogen stimuli. 



125 



The data were analyzed for statistically significant group distributional 
differences using the Kolmogorov-Smlrnov two-sample test. The analysis of the 
immunological cell count data showed no statistically significant differences. 
These cell count data are shown in Table ^'^. 



SELECTED PERCENTILES AND P VALUE FbR KOLMOGOROV-SMIRNOV TESTING 
OF NUMBERS OF SURFACE MARKER POSITIVE CELLS (THOUSANDS/MM^) 



Group 



10< 



50t 



P Value 

(comparing 

distributions) 



'3 
TLC» 



RH 
Coo 


235 

1UU 


0.70 
0.77 


1.25 
1.23 


1.96 
2.02 


0.74 


RH 
Com 


233 


0.70 
0.73 


1.27 
1.28 


1.96 
2.13 


0.39 


RH 
Com 


231 
1H7 


0.40 
0.48 


0.79 
0.78 


1.25 
1.42 


0.81 


RH 
Com 


235 

117 


0.30 
0.28 


0.57 
0.60 


0.99 
1.17 


0.34 


RH 
Com 


235 
1H7 


0.023 
0.022 


0.071 
0.071 


0.188 
0.247 


0.097 


RH 
Com 


290 
177 


1.34 
1.35 


1.92 
1.91 


2.54 
2.74 


0.63 



•Total lymphocyte count 



23 



83-529 95-5 



126 



statistical testing of the four stlnulatlon and two control oeasurements 
assessing lymphocyte functional ability Is shown in Table 15. 



TABLE 15. KOLMOGOROV-SMIRNOV TESTING OF T AND B CELL FUNCTION DATA: 
THYMIDINE INCORPORATION MEASURED AS COUNTS/MIN 



Variable 


Group 


N 


10* 


Percentiles 
50t 


90t 


P Value 


Control #1 


RH 
Coa 


279 
168 


1U0 
138 


37H 
UH8 


1.320 
1.483 


0.20 


After ConA 


RH 
Com 


279 
168 


17.7'»1 
13.596 


5'».190 
58,39'» 


91,72« 
99, ion 


0.38 


After PHA 


RH 
Com 


279 
168 


33,027 
30.^3 


79,3'«2 
81,339 


130,06'* 
135.684 


0.51 


Control #2 


RH 
Com 


27 H 
168 


132 
142 


388 

non 


917 
1.079 


0.85 


After PW 


RH 

Com 


27'< 
168 


12,700 
12.232 


29,623 
27,916 


58,288 
53,662 


0.64 


After TT 


RH 
Com 


27 H 
168 


866 
1,001 


3.726 
3.719 


13.979 
16.058 


0.81 



ConA - ooncanavallin A 
PHA - phytohemagglutin 
PW - pokeweed mitogen 
TT - tetenus toxoid. 



No statistically significant group differences are noted In these T and B 
cell function data. High laboratory variability and small sample sizes led to 
the decision to not use exposure index analyses with the immunological data. 
The control #1 and control #2 variables represent the unstimulated activity of 
the T cells. 



Endocrinological Effects 

Working with liver homogenates taken from adult male Wlstar rats, 
Nienstedt and colleagues^^ showed that TCDD reduced the catabollsm of testos- 
terone. Hook and colleagues^ also reported reduced metabolism of testos- 
terone. These reports would suggest that elevated testosterone levels could 
be observed in a recently dioxin-exposed population. 



127 



Ba3tomsky55 observed serum Tj, levels to be one-half of normal In TCDD- 
treated animals, but serum T^ was elevated by 50J. Sephadex uotake of T, was 
statistically significantly decreased. Potter and colleagues^" observed serum 
levels of T^ to fall to tSt of pair-fed controls in TCDD-dosed rats. However, 
no statistically significant change in serum T^ occurred. These authors also 
noted hypoglycemia after a single intraperitoneal dose of TCOO. Rozman and 
colleagues" emphasize the potentially important role of thyroid hormones in 
certain expressions of TCDO toxicity. Specifically, athyroid rats showed a 
markedly decreased mortality rate and less weight loss than nonthyroidec- 
tomized or thyroidectomized but euthyroid controls. 

In the endocrinological portion of the AFHS, five clinical variables were 
studied: T, uptake, serum Ti,, free thyroxine index (FTI), 2-hr postprandial 
glucose, and serum testosterone. One statistical analysis of these variables 
examined the number of participants below, in, or above the variables' normal 
ranges. This analysis is summarized in Table 16. Statistically significant 
difference is seen in these data for the Tj uptake comparison. The Ranch Hand 
group was also contrasted with the comparison group in terms of the five 
endocrinological variables using analysis of covariance, adjusting for age and 
percent body fat. These analyses are summarized in Table 17. Three group 
differences are noted in these analyses. In both the Ranch Hand and compari- 
son groups, a decrease in T, uptake is observed with advancing age, but the 
slope is -0.0068J per year In the comparison group and -0.0195J per year in 
the Ranch Hand group, and this group difference was statistically significant 
(p-0.026). Two-hour postprandial glucose levels increase with age in both the 
Ranch Hand and comparison groups, but the rate of increase is 1.53 mg/dl per 
year in the Ranch Hand group and 0.77 mg/dl per year in the comparison group 
(p-0.006). Lastly, Ranch Hands show a higher (but not statistically signifi- 
cant) testosterone level than do comparisons. Both increasing age and body , 
fat were found to be associated with decreasing testosterone levels to the 
same extent in both groups. 



128 



TABLE 16. UNADJUSTED PERCEMTACES FOR FIVE ENDOCRINOLOGICAL VARIABLES 
BY VARIABLE LEVEL AND CROUP 



Variable 


Croup 


N 


Low 


Variable Level 

Normal High 


P Value For 
Croup Difference 


T, Uptake 


RH 
Com 


1,032 
767 


5.72« 


93.'»1t 
91 .26$ 


0.87J 
0.26t 


0.020 


(ug/dl) 


RH 
Com 


1.033 
767 


O.IOt 
0.39X 


99.13J 
99.22J 


0.77J 
0.39t 


0.250 


FTI 


RH 

Com 


1,033 
767 


O.OOX 
0.261 


99.71$ 
99.7'»« 


0.291 
O.OOX 


0.085 


2-hr 
Glucose 
(mg/dl) 


RH 
Com 


I.OUO 
770 


NA 
NA 


8U.81$ 
82.73t 


15.19J 
17.27J 


0.23'* 


Testosterone 
(ng/dl) 


RH 
Com 


1,03'» 
769 


t.93J 
6.37X 


94.58X 
93.11J 


0.48S 
0.52J 


0.'41iJ 



26 



129 



TABLE 17. RANCH HAND COMPARISON GROUP MEANS OF ENDOCRINE VARIABLES 



Variable Group 



UnadJ . 
Mean 



Value For 
Unadj. Adjusted 
Means Mean 



Value For Remarks About 
Adjusted Adjusting 
Means Covarlates 



Uptake 
(J) 


RH 
Com 


1.037 
770 


30.28 
30. 1« 


0.21 






Group-by-age 

interaction 

(p-0.026) 


(ug/dl) 


RH 
Com 


1.038 
770 


8. 46 
8.39 


0.31 


8.45 
8.39 


0.38 




FTI 


RH 
Com 


1.038 
770 


2.54 
2.51 


0.07 


2.54 
2.51 


0.13 




2-hr 
Glucose 
(mg/dl) 


RH 
Com 


1.045 
773 


104 
102 


0.37 


» 


» 


Group-by-age 
interaction 
(p-0.006) 



Testos- 


RH 


1.039 


654 


terone 








(ng/dl) 


Com 


772 


634 



652 
637 



0.06 



•Signifies interaction present rendering group means noninformative. 



Mortality 



Administration of single doses of dioxin to animals can result in lethal- 
ity with marked species differences being observed.*^ Repeated dally doses 
can also lead to death. No studies with large numbers of animals (for 
instance, with 100 control and 100 exposed animals) are being conducted where 
the possibility of life shortening by very low doses of dioxin can be evalu- 
ated. 



The Australian government proYldes a very complex report addressing 
mortality among Vietnam veterans." Infantry exhibited a relative mortality 
rate of 0.96 with 95J confidence interval from 0.7 to 1.3. Engineers exhib- 
ited a relative mortality rate of 2.5 (confidence Interval 1.4 to 4.0); armour 
and artillery, 1.06 (confidence interval 0.7 to 1.7); veterans with minor 
field presence, 1.5 (confidence interval 0.9 to 2.6); and non-field corps, 
1.01 (confidence Interval 0.7 to 1.5). Thus, only the engineers exhibited a 
statistically significant difference (p-0.001), and that difference involved 
increased Vietnam veteran mortality. 



130 



In the AFHS, cumulative mortality as of 31 December 198t displays no 
statistically significant overall Ranch Hand-comparison differences. Summary 
counts of death and age standardized mortality ratios (SMR) by rank and occu- 
pation are given in Table 18. 



TABLE 18. SUMMARY COUNTS. SMRs AND P VALUES FOR DEATH BY RANK AND OCCUPATION 



Rank 


Ranch Hand 
At Risk Dead 


Rate 


Comparison 
At Risk Dead 


Rate 


SMR 


P Value 


Officers 
Enlisted 


U66 
791 


16 
39 


.034 
.0M9 


2278 
3893 


98 
187 


.01*3 
.018 


.791 
1.03 


.37 
.89 


Occupation 


















Flying 
Ground 


6M6 
611 


31 


.037 
.051 


3163 
3008 


161 
12U 


.051 
.01*1 


.726 
1.23 


.13 
.33 



Further study of these mortality data discloses complex patterns with 
date of birth (which is related to date of service in Vietnam) and date of 
death. 



In this report, eleven clinical areas have been emphasized based on a 
clinical toxicological profile developed from the literature concerning animal 
and human responses to dioxin and availability of data in the AFHS. Table 19 
lists the general toxicological effects anticipated on the basis of the liter- 
ature and also summarizes Ranch Hand findings. The toxicological profile we 
have developed from the literature certainly has an element of subjectivity as 
articles were selected and interpreted from a very large literature. Simi- 
larly, each observation in the AFHS can be challenged, and some specific 
caveats have already been mentioned. 



28 



131 



TABLE 19. SUMMARY OF FINDINGS* 



Toxlcologioal Effect 
Suggested by Animal and Observation In 
Human Literature on Dloxln AFHS 



Weight Loss o 

Increased Neoplasia ♦ 

Increased Birth Defects ♦ 

Neurological Changes o 

Psychological Changes *■ 

Hepatotoxlclty ♦ 

Chloracne o 

Cardiovascular Changes *■ 

Immunological Deficits o 

Endocrine Changes ♦/- 

Increased Mortality o 



^o" indicates no group differences observed 

'♦" indicates group difference observed in expected direction 

»-" indicates group difference observed but in opposite direction 



At this time one cannot ascribe the observed group differences to an 
effect of dioxin. One cannot implicate dioxin for at least four reasons: (a) 
the exposure index completely failed to demonstrate any association between 
increased exposure and increasing adverse outcome; (b) the full clinical pro- 
file for dioxin was not realized with the absence of chloracne being particu- 
larly noteworthy; (o) uninvestigated confounding variables remain for several 
of the target clinical endpoints, and resolution of these issues may alter the 
observed group differences; and (d) the effect of multiple statistical testing 
is not well defined. 

However, the AFHS does not exonerate dioxin as a causative agent of these 
group differences. This conclusion is supported by three reasons: (a) in six 
of eleven clinical variables, statistically significant group differences 
occurred, and in five of these six Instances the group differences were In the 
direction of expected dioxin effects; (b) uninvestigated confounding variables 
remain for several of the targeted clinical endpoints and resolution of these 
Issues could alter group differences; and (c) the currently available exposure 
Index is only an indication of exposure with unknown precision. 

The overall probability of obtaining the AFHS results under the hypoth- 
esis of no group difference Is not known. The summary in Table 19 cannot be 
used for statistical Inference at this time because the table summarizes the 
results of hundreds of potentially correlated tests of significance. Further 
clarification of the role of dioxin In human health must await the results of 
the follow-up phases of the AFHS and other ongoing epidemiologic studies of 
dioxln-exposed groups. 



132 



ACKNOWLEOGMENT 



r thank Ms Edith E. Wood for her professional help in retrieving and 
organizing the extensive literature review summarized in this report. 



1. Lathrop GD, Wolfe WH, Albanese RA, et al: An Epidemiological Investigation 
of Health Effects in Air Force Personnel Following Exposure to Herbicides: 
Baseline Morbidity Study Results. USAF School of Aerospace Medicine Report, 
Available from NTIS, Springfield, VA, 1984. 

2. Lathrop GD, 'Wolfe WH, Albanese RA, et al: Epidemiologic Investigation of 
Health Effects in Air Force Personnel Following Exposure to Herbicides: Study 
Protocol. USAF School of Aerospace Medicine Technical Report 82-tiJ, Available 
from NTIS, Springfield, VA, 1982. 

3. Lathrop GD, Moynahan PM, Albanese RA, et al: Epidemiologic Investigation of 
Health Effects in Air Force Personnel Following Exposure to Herbicides: Base- 
line Questionnaires. USAF School of Aerospace Medicine Technical Report 82-H2, 
Available from NTIS, Springfield, VA, 1982. 

I. McNulty WP: Toxicity of 2,3,7,8-Tetrachlorodibenzo-p-dioxin for Rhesus 
Monkeys: Brief Report. Bull Environ Contam Toxicol 1977:18,1:108-109. 

5. Case AA, Coffman JR: Waste Oil; Toxic for Horses. Vet Clin North Am 
1973:3:273-277. 

6. Carter CD, Kimbrough RD, Llddle JA, et al: Tetrachlorodibenzodioxin: An 
Accidental Poisoning Episode in Horse Arenas. Science 1975:1 88 :738-7tO. 

7. Chapman DE, Schiller CM: Dose-Related Effects of 2,3,7,8-Tetrachloro- 
dibenzo-p-dioxin (TCDD) in C57BL/6J and DBA/2J Mice. Toxicol Appl Pharmacol 
1985:78,1 :1H7-157. 

3. Seefeld MD, Peterson RE: Starvation-Like Syndrome and 2,3,7,8-Tetrachloro- 
dibenzo-P-Dloxin: New Ideas on the Mode of Action at the Whole Animal Level, 
in Proc Conf Environ Toxicol 1982:237-249. 

9. Oliver RM: Toxic effects of 2,3,7,8 tetrachlorodlbenzo 1,4 dioxin in labo- 
ratory workers. Br J Ind Med 1975:32:49-53. 

10. Hogdon JA, Marcinik EJ. Unpublished Data. Department of the Navy, Naval 
Health Research Center, San Diego, 1983. 

II. Jackson WT: Regulation of Mitosis, III. Cytological Effects of 2,4,5- 
Trichlorophenoxyacetic Acid and of Dioxin Contaminants in 2,4,5-T Formula- 
tions. J Cell Sci 1972:10:15-25. 



133 



12. Koclba RJ, Keyes DC, Beyer JE, et al: Results of a Two-lfear Chronic 
Toxicity and Oncogenicity Study of 2,3.7,8-Tetraclilorodlbenzo-p-Dloxin in 
Rata. Toxicol Appl Pharmacol 1978; 16: 279-303. 

13. Koupl RE, Rude TH, Joglekar R, et al: 2,3,7,8-Tetrachlorodlbenzo-p-dloxin 
as Cocarclnogen Causing 3-Methylcholanthrene-inltiated Subcutaneous Tumors In 
Mice Genetically "Nonresponsive" at Ah Locus. Cancer Res 1978;38: 2777-2783. 

14. OlGiovanni J. Berry DL, Gleason CL. et al: Time-dependent Inhibition by 
2,3.7,8-Tetrachlorodibenzo-p-dioxin of Skin Tumorigenesis with Polycyclic 
Hydrocarbons. Cancer Res 1980;40:1580-1587. 

15. Coggon D, Acheson ED: Do Phenoxy Herbicides Cause Cancer in Man? The 
Lancet 1982;1 :1057-1059. 

16. Hay A: The Chemical Scythe. Lessons of 2,U,5-T and Dioxin. Plenum Press, 
NY, 1982. 

17. Green S, Moreland F, Sheu C: Cytogenetic Effect of 2,3,7,8-Tetrachloro- 
dlbenzo-p-dioxin on Rat Bone Marrow Cells. FDA By-Llnes 1977:7,6:292-294. 

18. Van Miller JP, Allen JR: Chronic Toxicity of 2,3.7,8-Tetrachlorodibenzo-p- 
Dloxin In Rats. Fed Proo Fed Am Soc Exp Biol 1977:36,1:396. 

19. Seller JP: Inhibition of Testicular DMA Synthesis by Chemical Mutagens and 
Carcinogens. Preliminary Results in the Validation of a Novel Short Term 
Test. Mutat Res 1977;46:305-310. 

20. Courtney KD, Moore JA: Teratology Studies with 2,4,5-Trlchlorophenoxy- 
acetic Acid and 2,3,7,8-Tetrachlorodlbenzo-P-dioxin. Toxicol Appl Pharmacol 
1971 ;20:396-403. 

21. Smith FA, Schwetz BA, Nltschke KD: Teratogenicity of 2,3.7,8-Tetrachloro- 
dibenzo-p-Dloxin in CF-1 Mice. Toxicol Appl Pharmacol 1976:38:517-523. 

22. Lamb JC, Moore JA, Marks TA: Evaluation of 2,4-Dichlorophenoxyacetlc Acid 
(2,4-D), 2,4,5-Trichlorophenoxyacetlc Acid (2,4,5-T), and 2,3,7,8-Tetrachloro- 
dlbenzo-p-dioxln (TCDD) Toxicity in C57BL/6 Mice: Reproduction and Fertility 
in Treated Male Mice and Evaluation of Congenital Malformations in Their Off- 
spring. National Toxicology Program Report-80-44, 1980. 

23. Hanlfy JA, Metcalf P, Nobbs CL, et al: Aerial Spraying of 2,4,5-T and 
Human Birth Malformations: An Epidemiological Investigation. Science 1981 ;212: 
349-351. 

24. Townsend JC, Bodner KM, Van Peenan PFD, et al: Survey of Reproductive 
Events of Wives of Employees Exposed to Chlorinated Dloxlns. Am J Epidemiol 
1982;115, 5:695-713. 

25. Donovan JW, Adena MA, Rose G, et al: Case-Control Study of Congenital 
Anomalies and Vietnam Service (Birth Defects Study). Australian Government 
Publishing Service, Canberra, 1983. 



134 



26. Erlckson JD, Mullnare J, MeClaln PW, et al: Vietnam Veterans' Risks for 
Fathering Babies with Birth Defects. JAMA 198'4:252, 7:903-912. 

27. Bishop YMM, Feinberg SE, Holland PW: Discrete Multivariate Analysis: 
Theory and Practice. The MIT Press, Cambridge MA, 1975. 

28. Pocchiari F, Silano V, Zampierl A: Human Health Effects From Accidental 
Release of Tetrachlorodibenzo-p-Dloxin (TCDD) at Seveso, Italy. Ann NY Acad 
Sci 1979:320:311-320. 

29. Elovaara E, Savolainen H, Parkki MG, et al: Neurochemical Effects of 
2,3.7,8-Tetrachlorodibenzo-p-Dlo)cln in Wistar and Cunn Rats. Res Coraraun Chem 
Pathol and Pharmacol 1977;l8,3:'«87-'49'». 

30. Creso E, DeMarino V, Donatelli L, et al: Meuropsychopharmacologlcal 
effects of TCDD. Boll Soc Intal Biol Sper 1978;5«, 17:1592-1596. 

31. Bauer H, Schulz KH, Splegelberg U: Berufllche Vergiftungen bei der 
Herstellung von Chlorphenol-Verbindungen [Occupational Intoxications in Manu- 
facturing Chlorphenol Compounds]. Archiv Gewerbepath 1961;18:538-555. 

32. Poland AP, Smith D: A Health Survey of Workers in a 2,H-D and 2,t,5-T 
Plant. Arch Environ Health 1971;22:316-327. 

33. Weber G, Luzl P, Resl L, et al: Natural History of TCDD-Induced Liver 
Lesions in Rats as Observed by Transmission Electron Microscopy During a 
32-Week Period after a Single Intraperitoneal Injection. J Toxicol Environ 
Health 1983:12:533-5'»0. 

31. King ME, Roesler AR: Subacute Intubation Study on Rats with the Compound 
2,3,7,8-Tetrachlorodioxin. IIT Res Inst Rep to EPA No IITRI-L6073-12. 

35. Gupta BN, Vos JG, Moore JA, et al: Pathologic Effects of 2,3,7,8- 
Tetrachlorodibenzo-p-dloxln in Laboratory Animals. Environ Health Perspect 
1973;5t125-140. 

36. Blelberg J, Wallen M, Brodkln R, et al: Industrially Acquired Porphyria. 
Arch Dermatol 1961;89:793-797. 

37. Sweeney GD, Jones KG, Cole FM, et al: Iron Deficiency Prevents Liver 
Toxicity of 2,3,7,8-Tetrachlorodibenzo-p-Dioxin. Science 1979:201:332-335. 

38. Sinclair PR, Granick S: Uroporphyrin Formation Induced by Chlorinated 
Hydrocarbons (Lindane, Polychlorlnated Blphenyls, Tetrachlorodlbenzo-p- 
Dioxin). Requirements for Endogenous Iron, Protein Synthesis and Drug- 
Metabolizing Activity. Biochem Biophys Res Commun 1971;6l ,1 :121-133. 

39. Smith AG, Francis JE, Kay SJE, et al: Hepatic Toxicity and Uroporphy- 
rinogen Decarboxylase Activity Following a Single Dose of 2,3,7,8-Tetrachloro- 
dibenzo-p-Dloxin to Mice. Biochem Pharmacol 1981:30,20:2825-2830. 

10. Manis J, Kim G: Stimulation of iron absorption by polychlorlnated aromatic 
hydrocarbons. Am J Physiol 1979:236:E763-E768. 



32 



135 



41 . May G: Chloracne from the accidental production of tetrachlorodlbenzo- 
dloxin. Br J Ind Med 1973;30:276-283. 

i»2. Bovey RW, Young AL: The Science of 2,1,5-T and Associated Phenoxy Herbi- 
cides. John Wiley and Sons, MY, 1980. 

U3. Albro PW. Corbett JT, Harris M, et al: Effects of 2,3.7,8-Tetraohloro- 
dlbenzo-p-Dloxln on Lipid Profiles In Tissue of the Fischer Rat. Chem Biol 
Interact 1978;23:315-330. 

>iH. Schmlttle SC, Edwards HM, Morris D: A Disorder of Chickens Probably Due to 
a Toxic Feed-Preliminary Report. J. Amer Vet Med Assoc 1958;132:216-219. 

45. Cantrell JS, Webb NC, Mabls AJ: The Identification and Crystal Structure 
of a Hydroperlcardlum-Produoing Factor: 1 ,2,3,7,8,9-Hexachlorodlbenzo-p- 
dloxln. Acta Crystallogr 1 969 ;B25: 150-1 56. 

46. Jlrasek L, Kalensky J, Kubec K, et al: Chlorakne, Porphyria cutanea tarda 
und andere Intoxlkatlonen durch Herblzlde. [Chloracne, porphyria cutane tarda 
and other herbicide Induced Intoxications.] Hautarzt 1976;27, 7:328-333. 

47. Moses M, Lllis R, Crow KD, et al: Health Status of Workers with Past 
Exposure to 2,3.7,8-Tetrachlorodlbenzo-p-dloxln In the Manufacture of 2,4,5- 
Trlchlorophenoxyacetlc Acid: Comparison of Findings With and Without 
Chloracne. Am J Ind Med 1984;5:161-182. 

48. Zack JA, Susklnd RR: The Mortality Experience of Workers Exposed to 
Tetrachlorodibenzodloxln in a Trlchlorophenol Process Accident. J Occup Med 
1980;22, 1:11-14. 

49. Clark DA, Gauldle J, Szewczuk MR, et al: Enhanced Suppressor Cell Activity 
as a Mechanism of Immunosuppression by 2,3.7,8-Tetrachlorodlbenzo-p-dioxin. 
Proc Soc Exp Biol Med 1981;168:290-299. 

50. Montovanl A, Vecchl A, Luini W, et al: Effect of 2,3,7,8-tetrachloro- 
dibenzo-p-dloxln on macrophage and natural killer cell-mediated cytotoxicity 
in mice. Bloraedicine 1980; 32, 4: 200-204. 

51. Van Logten MJ, Gupta BN, MoConnell EE, et al: Role of the Endocrine System 
In the Action of 2,3,7,8-Tetrachlorodibenzo-p-Dloxin (TCDD) on the Thymus. 
Toxicology 1980;15:135-144. 

52. Clark DA, Sweeney G, Safe S, et al: Cellular and genetic basis for 
suppression of cytotoxic T cell generation by haloaromatic hydrocarbons. 
Iramunopharmacology 1 983 ;6 ,2 : 1 43-1 53 . 

53. Nienstedt W, Parkki M, Uotila P, et al: Effect of 2,3,7,8-Tetrachloro- 
dlbenzo-p-Dioxin on the Hepatic Metabolism of Testosterone in the Rat. Toxi- 
cology 1979:13:233-236. 

54. Hook GER, Orton TC, Moore JA, et al: 2,3.7,8-Tetrachlorodibenzo-p-Dloxln- 
Induced Changes in the Hydroxylation of Biphenyl by Rat Liver Microsomes. 
Biochem Pharmacol 1975;24:335-340. 



136 



55. Bastooaky CH: Enhanced Thyroxine Metabollsn and-Hlgh Uptake Colters In 
Rats After a Single Dose of 2,3.7,8-Tetrachlorodlbenzo-p-Dloxln. Endocrinology 
1977;101:292-296. 

56. Potter CL, Slpes IC, Russel DH: Hypothyroxinemla and Hypothermia In Rats 
In Response to 2,3,7,8-Tetrachlorodlbenzo-p-dloxln Administration. Toxicol 
Appl Pharmacol 1983:69:89-95. 

57. Rozman K, Rozman T, Grelm H: Effect of Thyroidectomy and Thyroxine on 
2,3.7,8-Tetrachlorodlbenzo-p-dloxln (TCDD) Induced Toxicity. Toxicol Appl 
Pharmacol 1981 j72: 372-376. 

58. Fett MJ, Dunn M, Adena MA, et al: Australian Veterans Health Studies (The 
Mortality Report), Part I. Australian Government Publishing Service, Canberra, 
1984. 



137 

PREPARED STATEMENT OF SENATOR FRANK H. MURKOWSKI 

Mr. Chairman, today we will explore some areas which we know very little 
about, but nonetheless may be very serious. Not much is known about the 
effects of chemical and biological agents of war. Even less is known of the 
effects of these agents on human reproduction. 

We will hear testimony from scientists and health care givers regarding 
toxins, radiation and chemicals and their possible connection to birth defects 
and reproductive afflictions. 

My primary consideration is that we focus on solutions and not sensational- 
ism. Scientists and medical professionals are better equipped to find these 
solutions than Congress. 

I must also express a concern that to some may seem trivial, but is one that 
this Committee must carefully consider. If science proves a connection between 
active duty military service and certain reproductive health problems, how do 
we on this Committee respond? It would seem like the Pentagon is the first line 
of prevention, if there is a problem. I fail to see how the Department of 
Veterans Affairs can deal effectively with hazards that may exist in combat 
theaters. 

We also must wonder whether the VA compensation and medical systems 
are equipped or authorized to deal with birth defects. 

I raise these concerns because I do not believe we ought to raise the 
expectations of the veterans, their spouses or children that this Committee or 
the Department of Veterans Affairs will either be the best equipped to stop a 
problem from occurring in the first place, or are able to deal effectively with 
consequences of these problems in the future, if there are any. 



APPENDIX 2.— PREPARED STATEMENTS OF 
WITNESSES 



Jadue C. Maxwell 
Dorectiir o^ ^tM^lir: Parents 
NATKXUVL ASaXIAnCN OF 
RADIAnOB SURVIVCRS 



RE: GENBnC CEFBCTS-ICNI2ING RADIATICN 



"Birth defects are the clearest exan^e of variation in the basic 
'building blocks' of life. They affect cdl hunan beings and 
potentially all living things." 

Dr. Uary Louise Buyse 



Definition of the term 'birth defect' is even now scientifically debated. 'Bom 
with' condition existing at birth. ' Yet many of the most recognizable birth defects 
do not even manifest themselves until the fourth or fifth decade of lifei 

A leading geneticist in his field told me that a clinician or doctor oould devote 
his entire career to just one defect becaise pf the ocnplexity of these cases. 

Over two thousand conditions have been catagorlzed, outlined and described, but 
over a third of the conditions do not fit any recognizable established diagnosis; We are 
seeing the appearance of two new ones per week. Oantrary to pnpiilar belief, fewer 
than 20% of these conditions a re inherited '. (This, despite the recent advances that 
'genetic or chronocxMcnal factors' play some part in most madical conditions). 

I4e are new experiencing over two hundred and fifty thousand birth defects each year 
whidi means 16« of all deliveries involve birth defects. Ten million anerican men and 
vaaen with birth defects reaching into the hundreds of thousnds are presenting a world 
wide medical challenge since the horrendous holocaust of Atooic warfare unleashing its' 
ionizing radiation upon our planet. 

Ttiat is what I wish to address today — the effects of ioninzing radiation on the 
Veterans and military personnel of Vtorld War H, the Atonic" Veterans. 

I an a member of the National Association of Radiation Survivors, and on that booard 
as a Director of Atonic Parents (of Genetically Iiifwired Oiildren). 

We have a seven thousand member data bank in which 20% of our radiation survivors 
have children with sane form of genetic defect. Of the four hundred and fifty two 
Atomic Veterans of Hiroshima and Nagasaki one hundred and seven of them have genetically 
inpaired offspring. Pot the papulation as a whole the 'norm' is 3 to 5%. The numbers 
of anomalies for these veterans are astronomical' 

My husband was one of those Atomic Veterans, and, as this is his story, I am going 
to introduce you to hiinn tell you of his bacgrcwndi and let him gxit 'faces' on five 
ot he ionizing radiation victims in his own words. 



(139) 



140 



Jacxie C. naxwexx 



rage 2- Geneuc Ueteccs 

Standing here before you is a Uteral'giant' of a oan, at 6'3 and 185 pounds 
Bctrwely handsane, charming -diairianatic and seU assured habitually hapw nan. 

He is Staff Sgt. Albert R. Maxwell of the 194th TtaJc Battalian Of the Uhited States 
Army. He ottered the service in 1939, stationed at Clark Field until the Pearl Harbor 
attack, and then to the defaise of Btaan util its' surrender of 1942. Participated in 
the Death March and surived forty three months or torture, enforced labor in copper mines 
and steel foundries (Mitsubishi) in camps from C&bantuan, O'Donnell, Santo Thomas, 
Bilibid Prison, Santo Domingo, Mukden, (Northern Oiina) and survived one of Maru 'Hell 
Ships, and sunk by our own subs because the ships were unmarked. His ship vas carrying 
fifteen hundred POW's — 'Al' vas one of only fifty five survivors. (He was, first and 
foremost a SURVIVCB and that is the way he thought of himself until the last day of his 
Ufe). 

The final two years of Al's iapriacraent uas spent at one of Japans' Hagoya 
oonoentratlon canps. There were ten such caaops, orlglnatiitg with Nagoya Onp fl 
at Nagoya itself and extending fron that area to Nagoya Caqp 40.0, located alnoBt 
at the epi-center of Hiroshima, Japan Al was incarcerated in Nagoya (^np K. 

on August 6, 1945 the P.O.W. ■« at Caap 96 heard the ti - emn rtn us boon 
and reverberation of the Atcmic blast (thought that it was our naval bcnbard- 
ment) . Oiey then witnessed the awesome spectacle of the Muahrocm dm ids and 
shorUy thereafter a 'dirty' stora ensued. (The 'blade rain'). On August 9, 
there was a faint repetition of the same rervarberatlng sound alcng the shoreline. 

The next day/ in oonjmction with twenty-four others, In groups of twelve, 
Al was sent-in on 'dean up' detail of three day intervals. Ttay were sent 
'somewhere 'in the Honshu pccvinoe, transported by track and traveling for over twelve 
ttdurs locrsp-to clear off the nibble and defads fron the roads leading to 
the outskirts of Hiroshima. Be noted in his diary "the dsvastaticn is terrible, 
it can't have been any natural disaster, nor bcEobing. Nothing I've read or 
heard of oould quialify as an explanation for this destruction. If It is their 
(Japanese) new secxet weapon, it must've backfired. I've got seme kind of rash 
all over my arms and legs." (The japanefw had explained the phencnonon they'd 
a 'their' new war weapon) . 



Als' camp was the very last of the prlscn canvas to be liberated. September 2n5 
through the 9th. They were then picked up by the USS Hospital Ship Hope along with 
dozens of others from Port to Port, eventually departing from Nagasaki, arriving 
Novemeber 15, 1945 in San Francisco. Al v>eighed 89 pounds. 

Upon returning home Al re-enlisted in the Service, seeking to persue the 
Army as his c ar e e r. However, on Decanber 18, 1947, after almost nine years service, 
he was given a m priical discharge with a 50« disability and thm reduced to 3(J%. 
His health began rapidly deteriorating, primarily due to the myriad diseases 
indigenous to all POW's who served in South Bast Asia. Betreme malnutritlan , ameohic 
parasitic diseases (which have never evwi been catagorlzed) D»gnue fever. Malaria, 
ravages of extreme malnutrition causing terrible ■'■""■1»'- spasms, vldent headaches 
and constant nightmares and consistent edema of the extremities. Residuals of beri-ber 
(wet and dry) eventually producing an enlarged heart (which is now finally recognized 
as service connected) as Ischemic heart disease. 

We met and married thirteen months later. 

THe following are excerpts from Al's diary. (I did not even know of it's existence 
until thirty-five years later). 



141 



^^, 



C^tJ:^ 



D<^ 



Father's Diary 

Albert Maxwell kept a diary and what foUows are excerpts which teU the story of h» c 



Dec. '^^ Wonderful neujs—l am no longer sfcn/e— 
and we are expecting a baby? Don't think 
either of us was ever so happv- 



July '48 IVe have the most beoutjM baby girl, tots 

// of bhck hair, enormous big blue eves and 

<£mples. 6 lbs. 7 ozs. Named her'Paulette' 

after Jackie's sweet Mom. Jackie had real 

(^cutties detiuerins- 

Our baby has a rare heart abnormality 
called "Tetra/ogy of Fallot." (A combina- 
tion of four concurrent symptoms of 
defects.) She also had a misplaced rectum 
which they have corrected surgicai/y. 
They houe told us she probably wont live 
much longer than a year. (Can't conceive 
of a life without her.) 

Aug. '48 They have put us through the wringer with 
J'-O all of their questions. They repeatedly ask- 
ed Jackie if she had uitdergone X-rays or 
been exposed to radiation. 

Oct. '48 Our baby is reoify a 'Daddy's girf. She 
dimples every tiirte I even look at h»r and 
gets so excited when I walk towards her 
that she hiccups. When I pick her up, she 
chuckles out loud and only three months 
oUL Has a tooth at this age. She has my 
whole heart in those tiny hands. 

Dec. '48 Paulette has pBed our whole ife with joy. 
She is such a charmer with those smiles 
and dimp/es and a very happy, surxny dis- 
position. A real gigg/er. Dainty. "S&m 



F 



Sept. '49 Lost our baby.' Desolate. She was ill one 

- --, day ond gone the next. Try to think of it as 

a blessing for her sake; so she won't have 

to suffer. But all I can think of is . . .She 

is GONE 

This pain surpasses anything I've ever 
endured. Am so worried about Jackie. 

Sept. '49 Sick. Nightmares, headaches this past 
whole week. Haven't slept since Paulette 
died. Sick. 
I've lost 20 pounds! 



Feb. SO We are going to have another baby. This 
n time rhey u/i// fake if by Ceosarean section 

for Jackie's sake and the baby's. 

June '58 8oby boy.' Husky little boy. Three (?) 
/y blonde hairs on his head. Weighs 8 lbs. 
10 ozs. Name Michael Birch Maxwell. 
Bom on his Grandfather's birthday. 

Weighed today at the hospitaL I've gained 
15 pounds. 

June '50 Against impossible odds, our baby has 
"tetralogy of fallot." Doctors say they've 
never known another such occurrence. 
We're stunned! Doctors have come from 
all over to examine both of us and Michael 
and Paulette's medical records trying to 
determine the possible cause. 

Questioned all older members of both 
families. (I'm youngest of seven children 
who've produced some 52 offspring, all of 
them normaL also 12 grandchildren, like- 
wise!) No history of any abnormalities- 
Jackie's family has genealogy, records and 
family histories going back 200 years with 
listing o/ ailments, cause of deaths, etc. 
and NO ABNORMALITIES. 

June "SO Some hope. Michael has an otherwise 
healthy body. They teU us not to give up 
hope. We'll try to prolong his life, hoping 
for a successful operation to be developed. 

I've had another attack of malaria. I finally 
went to the V.A Hospital. Att they did was 
examine me and send me to Dr. C.S. He 
said my left eye seemed very diaiated with 
a diminished vibratory sense, able to 
sense mooemenf only. 

Aug. '50 They'ue been monitoring Mikie carefully 
and discovered that he has premature 
showings of hydrocephalus. They are 
going to operate on him. remove a kidney 
and insert a catheter that will draw off 
the excess fluid from the brain. It's ternbly 
risky because of his heart. 



Sept '50 Operation is a complete success. They 



142 



Page i' Genetic Defects 



Jaclue C. MaxweU 
Testincrv re: icniz- 
zing radiation. 



are showing films of it at the Boston Medi- 
cal Convention. 

Mikie will be hospitalized for three months. 
I've gotten a night job to try to supplement 
our income. He's going to have 
the best care possible. 

July "51 Another baby girV (Not planned.) A per- 
fect baby girl, perfect heart, the most 
gorgeous baby I've ever seen! The whole 
hospital staff thinks so too. Doctors have 
come in from all over to examine her be- 
cause of the condition of our last two 
babies. They are all so thrilled for us. She 
is such a doll (looks like her Mother). Has 
little dark curls, btg dark eyes and dimples 
all over her body. She only weighed 5 lbs. 
14 ozs., but she's leally a 'chubb'. r? '^t^ 

We are all on 'cloud 9'. But for some 
reason Jackie is convinced that all is not 
right, even though the doctors have 
assured us that she is perfect. Named her 
Michele. 

July 31 Our perfect baby giri (Med today. Doctors 
were all stunned. She developed breathing 
problems and quite literally smothered to 
death. Diagnosis "Atelectasis' of the 
lungs. Another congenifoi abnormality! 
The doctors did say that at least it proi.ea 
we could have a normal baby f God she 
fought so, hard tc Uve. let' "her 
Sleep well. Your d^dy lov«s vou. 
precious little Mlcheiev 

July "51 I've been so bitter, so full of hurt and imiii 
If it weren't for Jackie and Mikie, I really 
wouldn't want to live! Life is so precious 
and hard to come by that I never thought 
I'd feel this way. But I do. Can't eat or 
sleep. The nightmares and headaches 
back again My heart feels lite 
it's being ripped out of my chest. 



Aug. "5 1 We "ne spent two whole days going over all 
records available to us. The doctors are 
baffled' They've said since there is no 
previous medical history on either side of 
abnormalities that rf ivot "yusf one of 



those things!! 



In reviewing my service medical records, 
they were truly upset that I hadn't m<.n. 



tioned my having been in Japan when the 
atorruc bombs were dropped there. 

Wanted to know if I had been in the area. 
(I had.) Whether I'd spent any time there. 
(1 had) Where I had worked in the area. 
(I had been detailed there to clean up 
debris.; Had I ingested any food or water 
while there. (I had) Had I had any ill ef 
fects man^est themselves durir^ that 
time. (I'd had an awful rash of some sort 
that came and went) 

Aug. SI In view of all the above, they strongly 
advised us not to have any more childrer\. 
We'd (or I'd) already deaded that because 
Jackie had almost lost her Bfe each time 
during the ceasareans. Her doctor was 
terribly concerned obouf her. 

July SS They have done a catheterization on 
Mikie prior to operating on him in Sept- 
ember. He's doing so u^efl now. Walking, 
talking, just learned to swim two weeks 
ago. We reaBy fluctuated concerning the 
heart operation, but we have decided to 
go ohcod with it. 

Aug. '55 Mtfcie was ill yesterday. Is gone today! 
(Just Bke Paulette!) We are both stUI'ina 
strange state of shoclc. He had beaten all 
the odds in cases Hke his for lorygeuity, 
progress, etc We'd tried never to get our 
hop« up for his future— but we've fought 
so long and hard to give him his chance 
(especially Jackie). I'm really concerned 
for her. Before she was the strong one. 
Not so this time. 

Tve had another attack of malaria. Head- 
aches fierce. 

Jan. '56 Jackie and I had the only senous quarrel 
of our married life. She wants another 
baby. I don't. Her doctor doesn't want us 
to even corvider it. Said he'd already told 
her that he wouldn't take care of her if she 
did become pregnant. That moybe she 
could go through rf again, but he couldn't! 

April "56 Jackie has convinced both me and the 
doctors to go along u,ifh her wishes. If she 



143 



Page 4- Genetic Defects 

has that much faith, I guess all of us should 
do likewise. First time she has felt that the 
baby would be alright. She will try to carry 
the baby ouer the 9 months to give it a bet- 
ter char\ce. The doctor worries about a 
possible rupture of the utehne wall, but is 
watchir\g her daily the last two momhs. 

Jan. '57 Robyn Kelly MaxwelU has arriued! Doc- 
tors all /one my wife. They'ue called our 
new little girl "Beauty's Beauty!" She •""'; 
2 days shy of 10 months. Weighed a whop- 
ping 10 pounds and looks fifcc a two month 
old baby. They've run every conceivable 
test on her. Everything is normal! She's 
darling, blue-blue eyes, red gold hair. 
HEALTHY— and all ours. My cup runneth 
ouer! Ill have to listen to "I told you so" 
the rest of my life. And to think 7' didn't 
want another baby. Thank Cod for her! 

Aug. '61 I am completely fatigued. Missed three 
weeks work. Extreme pain in chest wall 
X-rayed. Not i 



Robyn has been so beautifully healthy 
we've decided to try again. Another 
beautiful dark haired baby girl. Jackie was 
unable to carry the baby the ten months 
that we had planned on. The baby was 
premature by two weeks. Weighed 5 lbs. 
10 ozs. Lived the same amount of time as 
Michele. Died with same ailment! Atelect- 
asis of tne lungs! 'Ber name wasTiS-", 
Reb^ca, we'KNCw'we'll see you a^n 
don t forget us, we won't forget 
you." 



Jackie C. Maxwell 
testimony lo-Rad 



We know now that it is the radi- 
ation that has devastated us. 

We are now informed and believers 



ite've madt ^.^ ^ ^ 

to work as long as it takes 

get the government to recognize 
the horrors of ionizing radia- 
tion upon all wtw are touched by 
It, specifically the 'unborn' as 
disasterous effects on the reprod- 
uctive systan. 

Whatever you may have heard or 
Believe 'THESE IS MO SAFE 
RADIATION LEVEL." 



We have worked since 1961 to bring 
awareness to American health organ- 
iations, the scientists and the 
It is now 1994: 



This WBS a 'nan aocng men, ' of intelligence and charm, \4x> oonnanded the love 
and respect of everyone who knew him. Who looked for the best in others, because 
he, himself, posessed these qualities, who shared his happy optoatstlc outlook with 
all of us creating peace and harmony with whomever he met, wherever he went. Who 
oould find challenges with hardships and adversity and went on to greater challenges 
seeming to find opportunities out of misfortune and refused to let circumstances defeat 
him. Be had a great belief that evry life has a purpose and meaning, and that it is 
always, 'always' worth living. As a man of integrity and principle he was always at 
peace with himslef . In the forty years we were married I never knew him to ever alanripr 
another hunan being, nor, ever, ever tell a Ue. He was raised with that oode of honor 
and never departed frcm it. He's had many articles, and books dedicated to him as the 
"Gentle Giant. ' 

JUst prior to his death, our daughter, Robin, was venting her (justifiable) anger 
at the 'government' for calling her father a liar, and in general 'railing' against 
this country and its* injustice, Al sat up in bed and said "don't you EVHl let oe hear 
say anything lUte that agedn. Our Qxistitution is divinely inspired, don't you ever 
forget that. Granted there are officials and adninistrators who are inept and mis- 
guided, to say the least. But if you were ever to find yourself in another country, 
for an exteided leingth of fime as an 'invited guest' (not a prisoner) you vculd get 
down and kiss the g iu u iid of this oountrv, and never vant to leave it aaain." 



144 



Page 5- Genetic Defects 



Jackie C. Maxwell 
Ionizing radiation 



Oir daughter vea openly sobbing then, said 'but look what the exposure did to you 

^rSIJ"^•{S^^^ ^^ ^."^ '^ '^''^ ^^^ y^' ^t'3 not worth it." 
Al repUed, honey, the truth will 'always' out, it may take tUne, but it will. And as 
long as you beUeve in your old Dad that's aU that is inpartant. If my Ufe hadn^ 
evolved the way it did, I would never have met your Man, nor had those diildrwTnar 
you— you stLU think it wasn't worth it?" -u-iuren, nor 

Thank you for this opportunity to keep my pledge to the most wonderful man I've 
ever known. lie suffered agonizingly and has waited a long, long time for the 
acknowledgement of such a "Hearing" to occur. 



JUiank you for listening with your hearts to seme of the 'real ' people behind 
the statistics. If ever I can be of assistance to you, please advise. 



Sincerely, 



J»ricie C. Maxwell 
Directar-Atomic Baroits 
NATIGNAL ASSCCTATICN CF RADIATICN SORVIVDRS 



Diary excerpts reprinted 
courtesy of ABDC. 



Editor's Note Albert Maxwell's diary vuas provided to ABDC by the National Associatnn of Radiation Survivors. 
Chances are only one in 10 milEon.births of having five out of six babies bom with abnormalities like those of the 
Maxwells" children. NARS is pressing for genetic studies of atomic veterans and their children. The Maxwell's only 
surviving child, Robyn, is now married and has recently had a perfect first graiKkhild. 



145 

PREPARED STATEMENT OF ALBERT G. PARRISH 

Thank you, Mr. Chairman and members of the Committee. I am honored 
and pleased to testify on the issue of reproductive hazards and radiation 
exposure during military service in the 1950s. 

First and foremost, let me start off by thanking you, Mr. Chairman and 
Members of the Committee, for holding tiiis important hearing today. 

We, the Forgotten 216th, which is made up of former members of the 216th 
Chemical Service Company, applaud you for taking the time and energy to 
examine this tremendously important issue. Former members of the 216th 
Chemical Service Company have waited a long time to share their experiences 
with reproductive problems linked to radiation exposure. It is better late than 
never. 

I also want to take this opportunity to thank Senator Paul Wellstone from 
my home state of Minnesota for his strong support and genuine concern. If it 
wasn't for his personal commitment and interest on this subject, I wouldn't be 
here today testifying before you. In February, the Senator helped us tell our 
story to Minnesotans and the U.S. Department of Veterans Affairs, and now he 
has helped us to tell our story to you and the nation. 

Introduction 

My name is Albert "Smoky" Parrish and I am the mayor of Hackensack, a 
small town in northern Minnesota. Ora, my wife of 44 years, and I have two 
daughters. One was bom before I was exposed to radiation, the other was 
adopted. For the past 40 years, I have been a proud member of American 
Legion Post #202 in Hackensack, Minnesota. 

I come before you today on behalf of the former members of the 216th 
Chemical Service Company. I will talk about our collective experiences, rather 
than just my own. I will share the views, and recommendations of the 
Forgotten 216th as they relate to this issue. 

Military Service & Exposure to Radiation 

I was drafted into the United States Army on December 3, 1950. I was 
proud to serve my country, but little did I know that I would be exposed to a 
great amount of radiation. I was stationed at the Rocky Mountain Arsenal in 
Derby, Colorado and served in the 216th Chemical Service Company. As a 
Corporal E-4, I was a crane operator and heavy truck driver. 

In March, 1952 I received orders to accompany the 216th Chemical Service 
Company to Mercury, Nevada to participate in Operation TUMBLER- 
SNAPPER. I think about 100 hundred Minnesotans were in the 216th Chemical 
Service Company. 

According to the attached Defense Nuclear Agency's letter, dated May 20, 
1994, to Senator Paul Wellstone: 

Operation TUMBLER-SNAPPER was a U.S. atmospheric nuclear test 
series conducted at the Nevada Test Site (NTS) from April 1 through 
June 20, 1952. ..The 216th Chemical Service Company was part of the 
On-Site Operations Department of the Radiological Safety (Rad-Safe) 



146 

Group during Operation TUMBLER-SNAPPER. The mission of the On- 
Site Operations Department was to implement the poUcies, directives and 
orders of the Director of the Rad-Safe Group (Operation TUMBLER- 
SNAPPER, Radiological Safety, Report to the Test Director WT-558 
(Del.), December, 1952). 

In other words, the basic mission of the 216th Chemical Service Company 
was to monitor the radiologically contaminated areas (including ground zero) 
immediately following detonation of the atomic bombs. The mission was also 
to support and brief other personnel involved in the testing, process and 
interpret the dosage readings, "man" the check points, locate the "fall-out," and 
monitor and decontaminate vehicles and recovery equipment returning from 
contaminated areas (U.S. Department of Commerce, National Technical 
Information Service, "Operation TUMBLER-SNAPPER 1952, June, 1982, page 
160). During these eight atomic tests, I was personally involved in some these 
types of duties. 

According to the government's own records, there were eight atomic 
detonations during Operation TUMBLER-SNAPPER that yielded a total of 104 
kilotons (U.S. Department of Commerce, National Technical Information 
Service, "Operation TUMBLER-SNAPPER 1952", June, 1982, page 30). 
Remember, one kiloton equals the approximate energy release of a one- 
thousand ton TNT explosion. Most people don't realize that the combined 
atomic blasts at Hiroshima and Nagasaki only yielded 36 kilotons {Atomic 
Veteran's Newsletter, NAAV, Winter 1993, P. 4). Therefore, we in the 216th 
were subjected to three times the amount of radiation than the personnel and 
citizens involved in the atomic bombs blasts in Japan. According to the 
National Association of Atomic Veterans, there were over 200 atmospheric 
atomic and hydrogen bomb tests conducted on Americans. There were only two 
on the Japanese. 

Lack of Safety Precautions 

In looking back at my service and in reading through the relevant documents 
I must conclude that the U.S. military and the Atomic Energy Commission did 
a very poor job of protecting us from unsafe levels of radiation. 

According to the figures on page 178 in the U.S. Department of Commerce 
report on Operation TUMBLER-SNAPPER, twelve men from the 216th were 
recorded as being overdosed on their film badge readings for exposure to 
radiation. That is about 10 percent of the 216th Chemical Service Company! 
Furthermore, about 25 percent of all the personnel who were overdosed in 
Operation TUMBLER-SNAPPER came from the 216th. At best, it seems that 
they were unconcerned about our safety or careless about their jobs. At worst, 
we may have been guinea pigs. 

To give an example of an unsafe decontamination practice, I will quote 
directly from a Defense Nuclear Agency report. "Personnel were brushed with 
brooms to remove contaminated dust when they returned from the trench area 
(U.S. Defense Nuclear Agency, DNA 6021f, page 77). The radiation dust 
particles brushed off the men were thrown into the air and subsequently 
ingested into their bodies where film badges couldn't record the dosages. So 
who knows how much radiation we actually ingested as we drove through the 
dusty desert. 



147 

The first atomic test shot titled "ABLE" was detonated only about 10 
Kilometers from Camp Mercury, where we lived for over three months. We did 
not wear film badges to measure the radiation, so we have no idea how much 
radiation we were exposed to while in camp. To give you a picture of our 
living conditions in the camp and how ill-protected we were, let me quote a 
letter I sent home dated April 25, 1952: 

I live in a hut with four others... So there are five of us in here. The 
walls are made of plywood with no windows and they have no roofing 
on them. Just a plywood roof So it doesn't keep anything out. Dust, rain, 
snow, gravel, or anything makes its home in the huts. 

It is swept out every morning and right after it's swept you can't step 
on the floor barefoot or your foot is black. There's no way of mopping 
it cause the water out here cost the army seven cents a gallon. So they 
really frown on the excess use of water. 

With unprotected living conditions like this, what bothers me the most is 
why they set off the first bomb only 10 kilometers from camp. The rest of the 
bombs were detonated at least 40 kilometers away. If they had been concerned 
about us they would have set the closer one off after they tested the more 
distant bombs. 

My Radiation Exposure and Reproductive Hazards 

Like I said before, my wife and I have two children. Our biological daughter 
was born before I was exposed to radiation in Nevada. After I returned from 
Nevada, my wife and I tried to have more children, but were unsuccessful. V^e 
had three stillborn babies and two miscarriages. Later, doctors told us that my 
sperm was unhealthy and we better stop trying to have children because it was 
too physically and emotionally demanding on my wife. The Department of 
Veterans Affairs wouldn't consider my 1989 claim for service-connection for 
these reproductive hazards because they stated they couldn't "consider (my 
wife's) miscarriage as a disability for (me)" (see attached document). This 
really didn't surprise me at the time, because our military records were sealed 
and classified. 

My only biological daughter who was born before I was exposed to 
radiation has been and still is completely healthy. 

After the stillbirths and miscarriages, doctors discovered that I had a tumor 
on the left testicle. It was removed and at the same time the doctors had to 
perform a vasectomy. 

As a side note, I would like to mention some of my other ailments I believe 
are linked to radiation exposure. These health problems include posterior 
subcapsular cataracts, benign tumor on roof of mouth, benign tumor on bottom 
of right foot, tumor on neck/spine, lung problems, and severe cluster headaches. 
I recently filed another claim for service-connected veterans' benefits for all of 
these conditions. I will wait to see what the VA's final decision is before I 
comment on their action. 



148 

Other Members of 216th Chemical Service Company & 
Reproductive Hazards 

I would like to take a few moments to tell you about the reproductive health 
struggles of some of the other members of the 216th Chemical Service 
Company. After Senator Wellstone brought a team of U.S. Department of 
Veterans Affairs experts to Minnesota last spring to meet with us, I realized we 
needed more information about the health of the former members of the 216th. 
So I wrote to as many of them as I could find around the country. About 45 
of them responded with an update on their health. And about 15 of them said 
they have had or are having reproductive health problems. 

I would like to give you a few more details about the reproductive health 
problems of some of these former members of the 216th. 

A friend and former member of the 216th has had a horrible history of 
reproductive health problems since being exposed to radiation. Here is a history 
of his six children: 

Child #1: bom September, 1955; still living 

Child #2: bom January, 1957; died, premature 

Child #3: bom January, 1958; died, premature 

Child #4: bom July, 1959; still living 

Child #5: bom February 1962; died, premature 

Child #6: bom March 1965; living, premature, diagnosed paranoid 
schizophrenic 

Another former member of the 216th, who will submit separate written 
testimony, has a daughter who at age 14 had breast tumors, at age 18 had 
cancer of the cervix, and at age 28 had major kidney problems. 

These and some other atomic veterans from Minnesota plan to submit 
written testimony for the official record of this hearing. 

My Recommendations on How to Respond to Reproductive 
Hazards of Atomic Veterans 

I strongly believe that atomic veterans and their families have waited much 
too long for recognition, compensation, health care, and information ft-om the 
military and the govemment. 

I applaud the Committee for its willingness to examine the issue of 
reproductive hazards, even though it has been over forty years since we were 
exposed to radiation. 

I know that the Committee has the huge task of responding to the health 
care and other needs of veterans from all eras and wars, including Vietnam and 
the Persian Gulf. I strongly believe that the Committee should do everything 
in its power to respond to the needs of all veterans. 

But, I plead with you, don't forget us just because we older and may have 
been involved in more top secret activities. Please don't let the atomic veterans 
slip through the cracks any longer. And please in the future don't allow our 



149 

military to expose its personnel to toxic substances such as radiation, agent 
orange, and chemicals. 

To respond to atomic veterans' reproductive health problems, I urge the 
Senate Veterans' Affairs Committee to: 

1) immediately fund a comprehensive, independent study to examine the 
health effects and consequences for family members of atomic veterans of 
exposure to ionizing radiation. I understand that this request has been made by 
atomic veterans at several Congressional hearings in the past. 

2) take immediate and appropriate action to service-connect and compensate 
atomic veterans and family members for reproductive problems. Of course, this 
type of action would have to be contingent upon the results of a scientific 
study. 

3) continue to examine all health-related problems linked to radiation 
exposure and expand the list of radiogenic service-connected conditions where 
appropriate. 

4) ensure that atomic veterans receive all relevant documentation and 
materials needed to support claims for veterans' benefits, including more 
accurate reconstructed dosage amounts. If need be, give the veteran exposed 
to radiation the benefit of the doubt and presume that the veteran was exposed 
to unsafe levels of radiation. 

Conclusion 

Again, on behalf of the members of the Forgotten 216th, we would like to 
thank the Committee and Senator Wellstone for the interest and support in our 
effort for equity and justice. We would also like to express our appreciation 
and thanks to the National Association of Atomic Veterans (NAAV) for their 
support and guidance. 

I would like to leave you with a quote taken from the NAAV's quarterly 
magazine. "The Atomic Veteran seeks no special favor... simply Justice." 

I would be pleased to answer any of your questions. Thank you, again. 

Bibliography 

Atomic Veteran's Newsletter, NAAV, vol. 15, No. 4, Winter 1993 

DD214 and related service records of Albert George Parrish, 5 Dec 51 to 2 
Dec 52 

Defense Nuclear Agency letter to United States Senator Paul David 
Wellstone, May 20, 1994 

DNA Fact Sheets, Defense Nuclear Agency, Public Affairs Office, 
"Background of NTPR Program," 1 March 1982; "Nuclear Test Personnel 
Review Program, Radiation Exposure in U.S. Atmospheric Nuclear Weapons 
Testing," January 1994; 'TSfuclear Test Personnel Review (NTPR)," Jan. 14, 
1994 

Los Angeles Examiner, VOL. XLDC— NO. 134, Wednesday, April 23, 1952, 
"GIs Stand Up to Giant A-Bomb in Closeup Nevada Shock Tesf 



150 

Los Angeles Times, VOL. LXXI, Wednesday morning, April 23, 1952, 
'Troops in Foxholes See A-Bomb Loose Violence" 

Operation TUMBLER-SNAPPER, Radiological Safety, Report to the Test 
Director WT-558 (Del.), December, 1952). 

U.S. Defense Nuclear Agency, Book Number 6020F, December 10, 1982, 
"SHOTS ABLE, BAKER, CHARLIE, DOG: The First Tests of Tumbler 
Snapper Series, 1 April to 1 May, 1952" 

U.S. Defense Nuclear Agency, DNA 602 IF, December 10, 1982 

"EASY, FOX, GEORGE, HOW: The Final tests of the Tumbler Snapper 
Series." 7 May to 5 June, 1952" 

U.S. Department of Commerce National Technical Information Service. 
June, 1982. ADA 122-242 "Operation Tumbler Snapper 1952." 




"You sball know the truth ana the truth shaJl set you free' WINT 

ATOMIC VETERAN' 

NEWSLETTER 

**S£E PAGE IS FOR WASHINGTON, D.C. CONVENTION* 



^1993 ^' 



Orville & Wanda Kelly, Co-Founders 



Dr. Oscar Rosen, Editor 



WE WERE THE VICTIMS OF RADIATIOI^ 

EXPERIMENTS TOO! 

THEY EXPOSED OVER 200,000 OF US 

IN OVER 200 ATMOSPHERSC 
ATOMIC AND HYDROGEN BOMB TESTS 

1945-1962 
THEY DELIBERATELY BOMBED US WBTH NUCLEAR 

WEAPONS AND EXPOSED US TO DEADLY 

RADIOACTIVITY TO SEE HOW IT WOULD AFFECT US 

AND OUR EQUIPMENT IN NUCLEAR WARFARE 

ON LAND, ON SEA AND IN THE AIR 

THEY DIDNT NEED OUR INFORMED CONSENT 

BECAUSE WE WERE UNDER MILITARY DISCIPLSNE 

THEY DEVALUED OUR iJVES TOO! 



TH 

THEY CRIPPLE 
THEY MADE 
THEY DENIED REP 



MADE 



US STERILE! 
AND KILLED OUR CHILSSTSE^! 
WIDOWS OF GUR WIVES! 
LTEDLY AND PUBLICLY T^A7 



THERE WAS EVER ANY DANGER! 



"SAY THE SAME UE OFTEN ES>JOt 

JoMph Paul Coebbals, NAZI Minister of I 



■H, THE PEOPLE WILL BELSEVS IT. 

r Enlightenment and Propaganda, 1933-1945 



^Uie Atomic Veteran seeksrw speciaC favor.. .simpty Justice 



152 



/[' c^-^fO'^^,1 fiu^r '■ r^/Z- ^^ A^/^;c l'ri-/> 



■^^M 3 



TESTS/OPERATIONS NUMBER OF DETONATIONS 

"All bombs arc atomic unless identified as MT( hydrogen or thermonuclear, Ed ) 



•Onek 
neglects 



1 equals the approximate energy release of a 



2 HYDROGEN BOMBS 



HIROSHIMA Japan 

NAGASAKI Japan 

CROSSROADS Pacific 

SANDSTONE Pacific 

RANGER Nevada 

GREENHOUSE Pacific 

BUSTER-JANGLE Nevada 

TUMBLER-SNAPPER Nevada 

IVY Pacific 

Shot Mike (First hydrogen bomb) 

Shot King 
UPSHOT-KNOTHOLE Nevada 11 

10th shot - Grable fired from 280 mm gun (15 KT) 

nth shot - aimax was 61 KT. (4 X the yield of the Hiroshima bomb. Ed.) 
CASTLE Pacific 6 hydrogen bombs 

TEAPC3T Nevada 14 

WIGWAM Pacific 1 

REDWING Pacific 17 

Yields given only for the following: (Yields of other 12 still classified) 

Isl -Lacrosse 

2nd - Cherokee (hydrogen bomb) 

3rd - Zuni (hydrogen bomb) 

6th - Seminole 

16th - Tewa (hydrogen bomb) 
PLUMBBOB Nevada 30 

Including: 

Franklin 

Lassen 

Wheeler 
HARDTACK I Pacific 34 

Yields given for only following 3 bombs: 

Cactus 



Koa 
Oak 

Teak (Operation Newsreel) Johnson Island area Mcgatc 
Orange (Operation Newsreel) Johnson Island area Megatc 
ARGUS 3 rocket shots - 
*Orville E Kelly witnessed over 20 of these detonations and died of c 

HARDTACK II NEVADA 37 

(A\i 37 -jitrt of very low yields although government published yields are regarded as 

DOMINIC 1 Pacific 23 

Christmas Island area 27 tests* 

Johnson Island area 9 tests* 

•These consisted largely of air drops and rocket shots Most nclds are given a 

DOMINIC II Nevada 4 

STORAX Pacific 10 



1 range 
1 range 



15 KT 

21 KT 

42 KT 
104 KT 

40 KT 
394 KT 

80 KT 

104 KT 

10 4 MT(megatons) 
SOO KT 
2514 KT 



158.09 MT 

176 KT 

30 KT 

(Total yield unknown) 

40 KT 
Sever.al MT 
3.5 MT 
13.7 KT 
5MT 
343.4 KT 



140 TONS 

5 TONS 

197 TONS 



18 KT 

1.37 MT 
8 9MT 



each 1-2 KT 
ijndingNAAVinl9: 

46 KT (Total) 
/ yniis, £i ; 

0-vrr 



Low, Infennt*di3te. .Mcgatt 



Low \n 

0-MT 



PAGE 4 



153 




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DEPARTMENT OF THE ARMY 
ice OF THE CMIEC CMBMICAl. OrFICCM 
WASHINGTON Z8. D. C. 






CML^ro-P 

SI'PJECTt Commendation 



U SepteidMr 195? 



Commanding Officer 
216th Chemical Service Con^jany 
Rocky Mountain Arsenal 
Denver, Colorado 









1. The following commendatory remarlo are quoted from 
a letter addressed to the Chief J Armed Forces Special Weapons 
Project by the Director of Military Application, United States 
Atomic Energy Commission: 

"The radiological safety .rorlc done by the 216th 
Chemical Service Company at Operations TOTffilER- , 
SNAfPEH contributed considerably to its success." 

This correspondence vras foxTrarded to the Department of the Army 
by the Chief, Armed Forces Special Weapons Project requesting 
that these remarks be brought to the attention of your unit. 

2. It is -.litii considerable pleasure that I pass them on 
to you and add to them my appreciation for a job well done. 



z^^\X^52 



E. F. BULLENE 
Uajor General, CSA 
Chief Chemical Officer 



,1 



155 



CMLMC-RM-14a (4 Sep 52) 1st Ind 

SUBJECT: Commendation 

216th Chemical Service Company, Rocky Mountain Arsenal, Denver 2, 
Colorado, 20 September 1952 

TO; Cpl Albert G. l^rrish, DS 55 038 034, 216th Chemical Service 
Company, Rocly Mountain Arsenal, Denver 2, Colorado 

1. It is with great pleasure that I forward to you the above 
letter of conmendation from the Chief Chemical Officer. 

2* I wish to add a personal statement of appreciation for 
your fine work during Operations TUMBLER-SHAPIER. The competent, 
dependable, and cooperative manner in which you performed your 
duties contributed greatly to the success of our assigned mission. 

3. Copies of this correspondence will be placed in your 
official 201 file. 



^^ZcytSyty 



WARREN B. POWER 
1st Lt Cml C 

Commanding 



156 




157 



— _ ^— 0«f«ns« Nuclear Ag«ncy 

a5&\i|;/7>Jtt 6801 Telegraph Roaa 

»^:^ — ^>^W Alexandria. Virginia 223103396 



WQ 




MAY 2 !394 



Honorable Paul David Wellstone 
United States Senate 
Washington. DC 20510-2303 



Dear Senator Wellstone: 



This is in further response to your inquiry of February 4, 1994, concerning your 
constituents from the Ann^s 2 1 6th Chemical Service Corps (sic) in Operation TUMBLER- 
SNAPPER. ^ 

The Defense Nuclear Agency (DNA), as the executive agent for the Department of 
Defense (DoD), initiated the Nuclear Test Personnel Review (NTPR) program early in 1978 to 
retrieve data and reconstrua the history of the U.S. atmospheric nuclear testing program and the 
post-war occupation of Hiroshima and Nagasaki, Japan. This program has many elements which 
are designed to assist the veterans who participated, to help the Department of Veterans Affairs 
(VA) in responding to claims, and to provide information to those concerned with the possible 
health effects of low-level ionizing radiation. Our program is described in more detail in the 
attached NTPR fact sheets"' 

Operation TUMBLER-SNAPPER was a U.S. atmospheric nuclear test series conducted 
at the Nevada Test Site (NTS) from April 1 through June 20, 1952 While available records do 
not identify a 216th Chemical Service Corps, Operation TUMBLER-SNAPPER. Radiological 
Safety. Report to the Test Director WT-558 (Del), indicates that the 216th Chemical Service 
Company was part of the On-Site Operations Department of the Radiological Safety Group 
during Operation TUMBLER-SNAPPER The mission of the On-Site Operations Department is 
described on pages 31 through 35 of that report (excerpts attached). 

All documents we hold concerning the 216th Chemical Service Company have been 
declassified and are available to the public. Hundreds of thousands of publications containing 
information pertinent to US atmospheric nuclear weapons tests have been declassified and are 
available at the Coordination and Information Center (CIC) of th? U.S. Department of Energy, 
Las Vegas, Nevada. The CIC is the government's major repository of unclassified materials on 
U.S. atmospheric nuclear testing, available to the public. The attached brochure describes the 
services and fee schedule of the CIC. Veterans of the 216th Chemical Service Company and 
members of their families are invited to contact CIC and to inquire how to obtain documents of 
interest to them. 



83-529 95-6 



158 



Historical reports concerning U.S. atmospheric nuclear testing are also available to the 
public through the National Technical Information Service (NTIS). Copies of these publications 
may be purchased through NTIS, 5285 Port Royal Road, Springfield, Virginia 22161. Attached is 
the current NTIS price list for historical volumes. Over 700 facilities nationwide, most of them 
libraries, have received copies of the historical volumes. Attached is a list of the facilities where 
individual historical reports are accessible to the general public for review. The Government has 
spent considerable resources to establish and disclose what happened during the U.S. atmospheric 
nuclear testing program as well as the U.S. occupation of Hiroshima and Nagasaki, Japan. 

Additionally, personnel service and medical records as well as unit morning reports and 
ofiBcer flight logs, are available through the National Personnel Records Center (NPRC), Military 
Personnel Records, 9700 Page Boulevard, St. Louis, Missouri 63 132. Veterans may request their 
individual records from NPRC using Standard Form 180 (copy attached). 

/ 

One of the purposes of our NTPR program is to provide data to the medical and scientific 
communities who are conducting studies on the potential relationship between exposure to 
external, low-level ionizing radiation and the subsequent incidence of disease. The initial studies 
were performed by the Centers for Disease Control (CDC), an agency of the Department of 
Health and Human Services. The results of the completed CDC study are attached. The National 
Academy of Sciences (NAS) continues to perform similar studies. For example, attached is a fact 
sheet titled "Follow-On Study of Atomic Veterans Underway." This fact sheet summarizes the 
limitations in the mortality study released by NAS in 1985, and outlines key issues that will be 
addressed in the follow-on study, expected to be completed in the fall 1997. NAS is also 
conducting a mortality study on participants of Operation CROSSROADS, the first peacetime 
atmospheric nuclear test series conducted in 1946. Spring 1996 is the anticipated time for the 
completion of the CROSSROADS study. 

We do not hold any verified morbidity or mortality information on participants of 
Operation TUMBLER-SNAPPER or any other U.S. atmospheric nuclear test series. Any 
reference to medical problems by veterans who write us is anecdotal and unverified (and 
protected by the Privacy Act of 1974). The VA may have some morbidity and mortality data in its 
role of adjudicating service-connected benefits. You may wish to contact Dr. Fran Murphy 
(1 16A), VA Central OflBce, 810 Vermont Avenue, Washington, DC. 20420. 

Through various legislation, entitlements have been established for compensation or for 
provision of health care to veterans of U.S. atmospheric nuclear testing, and of the occupation of 
Hiroshima or Nagasaki, including "Veterans' Health Care, Training and Small Business Loan Act 
of 1981" (Public Law 97-72); "Veterans' Dioxin and Radiation Exposure Compensation Standards 
Act" of 1984 (Public Law 98-542); "Radiation-Exposed Veterans Compensation Act of 1988" 
(Public Law 100-321); and "Veterans' Radiation Exposure Amendments of 1992" (Public Law 
102-578). These laws authorize the VA to provide medical care and to pay compensation benefits 
to certain veterans who were exposed to ionizing radiation while in military service, and 
dependency and indemnity compensation to certain survivors. Attached is a VA Radiation 
Information for Veterans sheet. 



159 



The VA has established a national radiation help line to assist veterans and their families 
with radiation disability claims. The VA's help line toll-free telephone number is 1-800-827-0365. 
All VA Regional OfiBces can also be contacted directly to inquire about and apply for VA benefits, 
by dialing 1-800-827-1000. 

The VA is solely responsible for determining Service-connected disabilities and 
administering benefits. DNA has no role in deciding the ultimate disposition of a claim or making 
related medical decisions. When requested, we provide the VA with information regarding an 
individual's activities and location(s) during the time in question, and with radiation exposure data 
where applicable. 

A Radiation Exposure Compensation Trust Fun4.has been established (October and 
November 1990) by the enactment of the Radiation Exposure Compensation Act (Public 
Law 101-426), as amended by the 1991 DoD Authorization Act (Public Law 101-510). Benefits 
may be available for on-site participants in U.S. atmospheric nuclear weapons tests if the 
individual has one of the diseases listed in the Act. 

The Trust Fund established by this law is being administered by the Department of Justice 
(DOT). Attached is a DOJ information sheet. Any questions regarding this legislation and its 
eligibility criteria should be directed to: 

Mr. Frank Krider 

U.S. Department of Justice 

P.O. Box 146, Ben Franklin Station 

Washington, DC. 20044-0416 

DOJ has also established a toll-free line to take calls (1-800-729-7327). 

The NTPR program invites direct correspondence from individuals who participated in the 
U.S. atmospheric nuclear testing program from 1945-1962 or in the occupation of Hiroshima or 
Nagasaki, Japan. They may write to us at: 

Defense Nuclear Agency 
ATTN: RAEM/NTPR 
6801 Telegraph Road 
Alexandria, Virginia 22310-3398 

We also maintain a toll-free line to take calls from veterans or their families (1-800-462-3683). 
Please feel free to refer other constituents to us for direct service either by mail or telephone. 



160 



I hope you find this information helpful. If I can be of any further assistance, please do 
not hesitate to contact me. 

Sincerely, 




ha^Smann 



jor Q gfieral, USAF 
Dirertor 



Attachments 

1. NTPR fact sheets (3) 

2. Radiological safety report excerpts 

3. CIC brochure 

4. NTIS price list 

5. Facilities Receiving NTPR vohimes 

6. SF180 

7. CDC study 

8. FoUow-on Study fact sheet 

9.. VA Radiation Information sheet 
10. DOJ Information Sheet 



161 



Fact 
Sheet 



Defense Nuclear Agency 

Public Affairs Office 
Washington, D.C 20305 



Subject: Nuclear Test Personnel Review (NTPR) 1 March 1982 

Background of NTPR Program 

Between 1945 and 1962 the Atomic Energy Commission (AEC) carried out some 235 atmospheric nuclear 
tests, principally in Nevada and the Pacific Ocean. An estimated 220,000 Department of Defense 
(DoD) personnel, military and civilian, were involved in this testing and many received low-level 
ionizing radiation exposures in the performance of various activities. Because the exposures gen- 
erally were well within established radiation exposure limits, there was no reason to expect any 
increased health risk. 

The first indication that former test participants might be experiencing adverse health effects 
possibly related to radiation exposure at the tests occurred in 1977. The Center for Disease 
Control (CDC) , as a result of its investigation of a leukemia case involving an individual who had 
participated in Shot SMOKY at the Nevada Test Site in 1957, became interested in the health status 
of all personnel who had been present at that shot. By late 1977, a DoD ad hoc committee, working 
together with CDC, had reconstructed a list of approximately 3200 DoD personnel present on the day 
of the SMOKY test and determined that some eight leukemia cases had occurred among the group. CDC 
calculations indicated the expected incidence of leukemia would be three to four cases. CDC 
undertook an epidemiological study of these personnel and subsequently identified an additional 
leukemia case. It should be noted that the cause of the leukeraias has not been determined to be 
related to radiation received at the test. In addition, no increased mortality from other forms of 
cancer has been observed in this group and the total number of deaths from all causes is essentially 
what would be normally expected. 

Responding to this initial indication of a possible health problem, DoD in December 1977 began a 
program of wide-ranging actions on behalf of the atmospheric nuclear test participants. The 
Defense Nuclear Agency (DNA) was appointed DoD's Executive Agent for this effort. The Nuclear Test 
Personnel Review (NTPR) program was established by DNA to carry out these responsibilities. 

Scope of NTPR Program 

The Nuclear Test Personnel Review Program specific tasks were to: 

• Compile a roster of the DoD personnel involved in the atmospheric nuclear tests. 

• Develop a history of each atmospheric nuclear event that involved DoD personnel, 
elated source documents which formerly bore a security 

• Provide estimates of atmospheric test radiation exposures — both as a check on film badge 
readings and as a substitute for them in those cases where badges were not worn or readings were not 
recorded or are not retrievable. 

• Establish personal contact with as many test participants as possible. 

• Identify those individuals who received a higher radiation dose than those doses recoiimended 
under current Federal guidelines for radiation workers, notify those individuals of their exposure 
level, and offer them free medical examinations at Government hospitals. 



162 



Fact 
Sheet 



Defense Nuclear Agency 

Public Affairs Office 

6801 Telegraph Road 

Alexandria. Va 22310-3398 

(703) 325-7095 

Facsimile Number (703) 325-2962 



January 1994 

Nuclear Test Personnel Review Program 
Radiation Exposure in U.S. Atmospheric Nuclear Weapons Testing 

Approximately 200,000 Department of Defense (DoD) military, 
civilian and contract personnel participated in U.S. nuclear 
tests that were conducted during the atmospheric test series, 
primarily in Nevada and the Pacific Ocean. Many were exposed to 
low levels of ionizing radiation in the performance of various 
activities. The doses generally were within the current federal 
occupational radiation guidance (5 rem per year) and averaged 
about 0.6 rem. Approximately 1,700 personnel received doses in 
excess of the current federal occupational radiation guidance. 

The Nuclear Test Personnel Review (NTPR) program, established by 
DoD in 1978 and administered by the Defense Nuclear Agency (DNA), 
provides test participants their recorded radiation exposux-e or 
assesses the most probable exposure. The basic means to measure 
dose from ionizing radiation at U.S. atmospheric nuclear tests 
was the film badge. Of the approximately 200,000 DoD 
participants in U.S. atmospheric nuclear tests, about 95,000 have 
film badge data available. The official repository for these 
records is maintained by the Reynolds Electrical and Engineering 
Company, a Department of Energy (formerly Atomic Energy 
Commission, AEC) contractor. Individual dose information is 
available from DNA. Requests for such information may originate 
from individuals, representatives authorized under the Privacy 
Act, the Department of Veterans Affairs (VA), or Congress. 

Until 1955, film badges were issued to some of the personnel in a 
unit, such as a platoon, ship or aircraft. If everyone in the 
unit was expected to receive similar exposures, only a few 



representati\ es might be badged . If some personnel were to 



perform functions not typical of the unit as a whole, then those 

personnel were individually badged. After 1955, DoD and AEC 

policy changed to require the badqinq of all participants . Some 
badges were environmentally damaged di 



result, a signiticant portion ot the NTPR ettort has focused on' 
assessing tne exposure ot personnel who were not issued film 
badges and those whose records are missing or incomplete. 

DNA considers all relevant circumstances when performing 
radiation exposure assessments. Assessments begin with the 
determination of individual or unit activities and the 
relationship of such activities to the radiological environment. 



163 



If records indicate the location of personnel and it is clear 
that they were not exposed to a radiological environment, their 
dose is judged to be zero. In units where some members had film 
badges with valid readings and others did not have badges, doses 
for the unbadged personnel who participated in similar activities 
are inferred from the doses of their badged counterparts. Where 
there are insufficient badges, or where a common relationship to 
the radiological environment does not exist, dose reconstructions 
are performed. 

Determination of No Dose Potential . DNA researches activities of 
an individual or his unit for the period of participation in an 
atmospheric nuclear test. Unit locations and movements are 
related to areas of radioactivity. If personnel were beyond the 
range of initial radiation (several miles) from nuclear 
detonations, did not experience fallout or enter a contaminated 
area, and did not come in contact with radioactive materials, 
they are judged to have received no radiation dose. 

Dose Based on Film Badges of Others . DNA uses film badge data 
from badged personnel to derive individual doses for unbadged 
personnel. A group of participants is identified who had a 
common activity and thus a similar potential for exposure to 
radiation. Identification of these homogeneous groups is based 
upon research of historical records, technical reports, or 
correspondence. Using standard statistical methods, the film 
badge data are examined along with a description of personnel 
activities to determine their validity for use in the 
reconstruction and their assignment to the entire group. Often 
the dose or time distribution of badge readings indicates that 
the group should be subdivided into more similar groups before 
proceeding further with the analysis. For each homogeneous 
group, the mean dose, variance and confidence limits are 
determined, and the upper limit dose is then assigned to unbadged 
personnel. This ensures that personnel are assigned doses that 
are higher than the average for the group based on uncertainties 

the activity description. If individuals cannot be associated 
with a specific homogeneous group, statistical derivation of dose 
is not used. 

Dose Calculation . DNA performs rigorous dose calculations when 
film badge data are" unavailable for any part (or all) of the 
exposure period. DNA also performs calculations if film badges 
are damaged and cannot yield reliable dose data, it unique" 

.activities are ascribed to specific individuals, or if neutron or 
internal radiation exposures to a target organ are indicated. 

^These calculations involve correlating the activities of an 
individual or unit with a fully characterized radiological 
environment . 

.The calculation of dose is a standard scientific practice used by 
health physicists when the entire circumstances of radiation 



164 



exposure require assessment. First, the conditions of exposure 
are reconstructed to include all known activities based on input 
from the individual as well as information from official reports 
and historical documents. The radiation environment is then 
characterized in time and space, and collated with the activities 
and locations of the unit or the individual. In addition to 
gamma radiation that has been measured by film badges, the 
radiation environment includes neutron radiation for close-in 
personnel and beta and alpha radiation for personnel whose 
activities indicate the possibility of inhalation or ingestion of 
radioactive materials. Finally, the intensity of the radiation 
is determined for the entire period of exposure, from which the 
total integrated dose is calculated. An uncertainty analysis, 
which considers the values of all parameters used, provides a 
measure of the confidence of the calculations. Existing 
dosimetry is then analyzed and compared with the calculated dose 
to further enhance the confidence of the calculations. Where the 
potential existed for inhalation or ingestion of radionuclides, 
internal dose commitments to the target organ are derived and 
provided to the VA and/or to the individual. These are doses 
accrued over a 50-year period after exposure which, when added to 
the film badge or calculated whole body dose, represent the total 
dose to the target organ specified. 

The above dose determination procedures have been reviewed by 
some of the country's leading scientists and were initially 
described in the Federal Register on May 20, 1982, and later 
amplified in the Federal Register on October 21, 1985. 
Subsequently, the National Academy of Sciences (NAS) completed a 
"Review of Methods Used to Assign Radiation Doses to Service 
Personnel at Nuclear Weapons Tests." The "NAS Committee on Dose 
Assignment and Reconstruction for Service Personnel at Nuclear 
Weapons Tests found that: 

"...the procedures used to estimate external radiation 
doses were reasonably sound.... The NTPR has developed 
procedures that permit satisfactory estimates to be 
made of the external doses received by these 
participants. There are uncertainties in the dose 
estimates, but it appears that 99 percent of the 
personnel received doses of less than 5 rems , which is 
approximately the average dose received by the general 
population during the last 30 years from exposure to 
natural radiation and the use of ionizing radiation 
during medical procedures ... .Although the committee 
concentrated only on methods, it found no evidence that 
the NTPR teams had been remiss in carrying out their 
mandate. If any bias exists in the estimates, it is 
probably a tendency to overestimate the most likely 
dose, especially for internal emitters or when the 
statistical procedure for assigning dose is used...." 



165 



DNA has developed the NTPR program to provide veterans with 
information relevant to their radiation exposure. Dose 
reconstruction, as noted above, is based on evaluation of 
available records. Test participants who can provide copies of 
personal records are invited to send them to DNA if it appears 
that their dose reconstruction is based on incomplete records. 
Further inquiries can be addressed to Defense Nuclear Agency, 
(ATTN: RAEM/NTPR), 6801 Telegraph Road, Alexandria, VA 22310- 
3398, or one may call 1-800-462-3683. In Virginia, call 
(collect) 703-285-5610. 



166 



Fact 
Sheet 



Defense Nuclear Agency 

Public Affairs Office 
6801 Telegraph Road 
Alexandria. Va 22310-3398 
(703) 325-7095 
^acsimM^^umbe^^703^25^962 



Jan. 14, 1994 

Nuclear Test Personnel Review (NTPR) 

The Defense Nuclear Agency (DNA) has been conducting a major 
program since 1978 to identify the approximately 200,000 
Department of Defense (DoD) military, civilian and contract 
personnel who participated in U.S. nuclear tests that were 
conducted during the atmospheric test series, primarily in Nevada 
and the Pacific Ocean. Since 1988, the program has also included 
an additional approximately 200,000 DoD personnel who 
participated in the post-war occupation of Hiroshima and 
Nagasaki, Japan. The NTPR program has involved intensive, high 
priority research of the broadest scope. Managed by a special 
office at DNA that is dedicated to identifying all such veterans, 
program personnel have compiled a register of DoD participants 
and the best av.ailable estimates of radiation exposure. In 
addition, program personnel have developed a history of each U.S. 
atmospheric nuclear event that involved DoD participants, 
collected and analyzed all known sources of recorded dosimetry 
and radiation data, and provided calculated doses in cases where 
recorded doses are unavailable or are incomplete. The program 
also supports studies to ascertain whether adverse health effects 
are being experienced by veterans that could be attributed to 
their participation. 

An extensive public outreach program has been conducted to ensure 
maximum interface with the thousands of test participants, to 
share with them the vast amount of data that has been collected 
on their behalf, and to advise them of the specifics of their 
individual involvement and their radiation exposure, estimated 
from available records. Over 100 archives nationwide have been 
researched for relevant information. Over 40 historical volumes 
and more than 25 analytical reports have been developed to 
provide details of each test and operation, and a reading room 
has been established at DNA Headquarters to assist in making 
these data available to the public. The Coordination and 
Information Center, a repository for over 300,000 documents for 
the U.S. nuclear test era, has been established in Las Vegas, NV, 
for public use. All NTPR reports also have been placed in 
libraries throughout the country as well as at Veterans 
Administration (VA) regional offices. To date, over 70,000 
participants or their representatives have contacted the program 
and have received a letter containing information that the NTPR 
has located on their participation. These contacts also have 
been followed up with mass mailings, whenever significant events 
involve the overall NTPR program. 



167 



This program has many elements which are designed to assist the 
veterans who participated, to help the Department of Veterans 
Affairs (VA) in responding to claims, and to provide information 
to those concerned with the possible health effects of low-level 
ionizing radiation. DNA has supported and continues to sponsor 
studies conducted by the National Academy of Sciences (NAS) to 
determine whether there is an increased disease specific 
mortality among nuclear test participants. 

Under the mandates of Public Laws 98-542, 100-321, 101-426, 101- 
510, 102-86 and 102-578, DNA continues to identify individuals 
who participated in U.S. atmospheric nuclear tests and the 
occupation of Hiroshima and Nagasaki, their radiation risk 
activities, and the resultant radiation doses, thereby 
facilitating VA health care and/or compensation of veterans as 
authorized by these laws. The VA advises that free medical 
examinations are available at VA facilities to any former 
military participant, as well as medical care for conditions that 
the VA considers to be related to exposure to ionizing radiation. 
Relatively few individuals (less than one percent of all 
participants) received doses in excess of today's federal 
guidance for occupational exposure, which is 5 rem per year. DNA 
has contacted each for whom an address could be found and 
encouraged them to undergo an examination. No adverse health 
effects attributable to radiation exposure have been detected 
among this unique higher dose group of veterans. 

Specific Accomplishments /Findings 

DNA continues to research the many issues surrounding the 
nation's atmospheric nuclear test program and the occupation of 
Hiroshima and Nagasaki. To date: 

o Over 400,000 participants have been identified and 
researched as to their specific involvement and their 
recorded radiation exposure. 

o Extensive dose reconstruction methodologies, developed to 
provide a comprehensive analysis of both external dose 
and internal dose commitment, have been published in the 
Federal Register and reviewed by many of the country's 
leading experts. These methodologies have been applied 
to most participating units as well as to individual 
circumstances of exposure to determine total doses to 
participating veterans. 

o Research indicates that doses to most DoD personnel were 
quite low, averaging about 0.624 rem. This is one- 
eighth the current federal guidance for allowable dose 
to radiation workers, which permits up to 5 rem per 
year. Scientists generally agree that even the current 
allowable dose carries a very low risk of causing 



168 



additional radiogenic disease above that normally 
observed in the general population. 

Hundreds of thousands of pages of data have been re- 
covered and researched, including over 1,000 basic 
test reports, many of which were declassified, re- 
printed, and indexed for public use. These documents are 
available at the Coordination and Information Center. 

Original dosimetry source documents have been and are 
still being re-examined for accuracy and completeness. 
Individual involvement is continually researched to 
ensure that all dose potential has been documented and 
included . 

At DNA's request, the National Academy of Sciences (NAS) 
conducted an extensive study of the mortality of more 
than 46,000 nuclear test participants. The study, 
"Mortality of Nuclear Weapons Test Participants," 
published in 1985, found "The total body of evidence we 
have reviewed cannot convincingly either affirm or deny 
that the higher than statistically expected incidence of 
leukemia among SMOKY participants (or of prostate cancer 
among REDWING participants) is the result of radiation 
exposure incident to the tests. However, when the data 
from all the tests are considered, there is no con sistent 
or statistically significant evidence tor an increase in 
leukemi a or o t her m alignant disease in nuclear test 
participants." One of the co-authors of 'ETiat study 
stressed that there were limitations in the study design 
that might affect the scope of the conclusions. Also, 
the cutoff year for collecting data for the first study 
was 1981. Since that time the data base has been 
refined, additional participants have been identified, 

and sev eral more years of mortali ty data have become 

availab le^ AccordingTy , ' DMA is sponsoring a follow-on 
study by NAS. The . folj^qwjonis expected to be completed 
in lat e 1997. An additional' NAS study, co-sponsored by 
the Vfi~ana"DNA, on the mortality of the 42,000 
participants at the 1946 Operation CROSSROADS is being 
conducted and will provide, in about two years, 

V ^ scientific information on deaths due to radiogenic 

disease in this large population. 

DNA is dedicated to providing a responsive, helpful program of 
historical research, dose determination, and individual support 
to ensure that veterans fully understand their involvement in 
U.S. atmospheric nuclear tests and in the occupation of 
Hiroshima/Nagasaki. Individual dose reconstructions, as noted 
above, are based on evaluations of records available from all 
sources. Participants who can provide copies of personal records 
are invited to send them to DNA if it appears that their dose 
reconstruction is based on incomplete records. Further inquiries 
can be addressed to Defense Nuclear Agency (ATTN: RAEM/NTPR), 
6801 Telegraph Road, Alexandria, Virginia 22310-3398, or one may 
call 1-800-462-3683. In Virginia call (collect) 703-285-5610. 



^^ 



169 




WANGER, JOAN REUNION HINTED 



COMPLETE 
RICES 



8 L. A jaUGE INDICTED 



|racfF|G/s Stand Up t,o Gtant A-Bomb 

in Closeup Nevada Shotk Test 

roops 3 MiJes . 
From Biggest Blast! 

Out of Foxholu 3 Seconds \ 
AfterHuge Explosion ' \ 




170 



iies From Blast Escape tjlarrn!^ 



A-ltiasi IScgM»i'<c(R 
Vifililc 4:iOJ)]lil<>fl 1 




171 




A-Bomb ibws 
a Smoke 1, 




Red Alert! And Pupils Crouch for 







172 



nm u 8 LA. pu yg 



Long 
^2000 Each 




173 




MUSHROOM CLEARLY Visibility 
SEEN AT MT. WILSON 









Cut 
byHazeatTime]' 
ot Atomic Test 






Raid Warning System 
Proves Partial Failure 



TROOPS SEE A-BOMB 
BLAST^IN NEJApA^ _^ 




.^.^V^s;;; AEC in Move 
«^_-««-.^. Tj^fg Industrializes;; 
~^'|[~^_ ^Atomic Power 




CALTECH MUM 
ON RECORDING 
OF BIG BLAST 



i^girTrr?^ Bouncing Balls 
X'S.J.^.f^ of Desert Dust 
~Z^zzsrT:.'. ^ll^fiveal Power 






fills: 






£-?iSS"=' 






174 



Pictures Record A-Bomb's (loud 
at Ranges From 10 to 200 Miles 








175 



JL8. 



Port I-WEO., APRIL 23, 19S2 



LosansclcsCimes 



A-BOMB EXPLOSION 



hills of the borde 

Their olive di 

liunctuated by 



lachuies. 



personnel arl\ancnig on a nn iht-l xipdei 



Tnirrra Dlsrcrnlble 

In il'e dimness of dawn, age- 
less Jo.^hua trees were shadowed ' 
scnlmelt "f coining violence | 
Rising ^.i.ovo them and faintly 
discerr.inle in the gray light 
stood Ire four 300-foot steel 
tower"; fiom which future deto- 
1 nation.^ will be touched off. 
I Lost in the distance at this 
ground hoiu- were the mounds of the 






lock 



lied' with the complex con- 
their mechanical 
brains electronically trained to 
record and evaluate later blasts. 
Half a mile behind the ob-j 
servers, scientists were at the 
bewildering instrument panel of 
the cootrol point readying thei 
explosion to come. From this! 
monolithic concrete building 
reached the coaxial nerve of the 



ftroyed by the blast, moved for- 
ward. 

Tactical Problems 
Swing 
military 

voted entirely to tactical prob- 
lems involved may be forthcom- 
ing. He stressea the necessity 
for such a plan as prerequisite 
to determining precisely how. 
intimate military personnel can ; experiment, 
become with atomic weapons. Clockwork Precision 

"That fireball was just anoth- 1 All that would happen would 
er piece of firepower to ui," he ; b^ controlled and known here, 
said. "We «ant to know howl wuh clockwork precision, the 
to use It best. Experience has I military contingent moved up 
taught us to move in close soon: nont through the chilly bleak- 
after artillery barrages. , nefs, 

■t'f^'^loP the means, Elements of the S2nd Airborn 

t how much .nuclear;. Division. Company B of the 

ndle and thatji67th Infantry Regiment. Com- 

neu- j pany C of the 135th Infanti-y 

"""■ ■ !Re,-iment, a.TJiatoon of medium 

Predawn Beginning [tanks from 

It began In the cold. 

Secked desert predawn wii 

progressive assembly of 



to learn j 
.vield we 
likes purely military 



lists, technicians, soldiers, offi- 
cial observers and the news- 
men who had heen invited for 
the first time to witness a test 
Mast at - the N'evada Proving 



Cavalry Regiment, a platoon of 
engineers from the 369th Engi- 
neer Amphibious Support Regi- 
ment, and a 6th Army medical 
detachment rolled in trucks to 
their position four miles beyond 
the observers. 

Bustling TTith AcUvlly 



As shot time neared. the cor- 
ner of the desert allotted to 
a.m. the motor caravan began newsmen bustled with activity 
threading through the darkness! novel to desert background. The 
of the desert from Las^Vegas^jD^ nob behind -he observers' sta- 
slled uith camera tii- 



iCampDes-f 
ei t Rock to\vai(l the broad 
wasteland cup of Yucca Basin. 

This was the 13lh atomic e.s. 
plosion here and the 26th. un- 
r -Hcially. by the United Stales, 

Interest had mounted steadily 
f'lice the "open shot" had been! 
announced. Wriiers and photog- 
raphers from all over the coun- 
try had convened to bring some- 
thing of the fury and signifi- 
cance of the event to the world. 

For the first nine, television 
cameras were to bring the awe- 
some spectacle into the living j. 
rooms of America after a tortu-|, 
riis round of arrangements to. 
eMahlish micrnuave facilities di-l 
iccilv from the site to Lo^ An- 



Ahead of them, corrcspond- 
rrits beat > strange aesTrt tattoo 
m their typewriters. And to one 
;ide an Army Signal Corps de- 
achment tended a row of 12 
elelype machines specially set 
ip to transmit copy to Las 
/egas. 

The muttering of the tele- 
ypes couldn't have been moM 
ncongnious as they told th'«s 
.vol Id the fantastic story ol 



helic 



ered 



cra2ily across ilm broad dr; ) -kc 
immediately ahead. Radioin;;iral 
safety men, garbed in coveralls, 
carrying heavy goggles and 
breathers, waited. Their bPoLi 
«ere wrapped in paper, giving 
the curious appearance of white 
arctics in tlie growing heat. 
Haze DifTuses Sunlight 
One hour 'from target time a 
slight haze di/Iused the bright 
sunlight over the firing area. 
The sky was cloudless except for 
a single patch of cumulus almost 
directly over ground zero. High 
above four B-50S touched the 



■ith 



ails 



gargantuan matches were being 
struck overhead. 

The 1500 military personnel to 
participate In the exercise 
now in place. The mice and goats 
and pigs which would be 
ficed to research were tethered 
down. At the 'observatii 
tion announcements cam 
increasing rapidity fro 
speaker system. 

A sense of readiness gripped 
the onlookers. 

Liaison Chief Speaks 

Then, over the rumble of r 
chinery and the undertone 
conversation, came the voice 
Dr. Gaelen L, Felt, technical 
liaison director. It issued f 
a loudspeaker, carrying his 



careful almost unconcerned 
voice of science, casually famU-, 
lar with Impending phenome-l 



vill be 



from 



the 



• control 
." he 1 



Daz 



ling 



ling 



rc.\ 



the desert. They 
of to\veringi lied the men who would crouch 

ijin fo.vholes for the detonation. 
nrinfS'the' ' I'"<c T.ofl), .o^Jat.le 
inUain-ringed I "^^^ '""8 line of vehicles tnade 
still motion-'" ''"" ''I'O"" streak acros.'!,the 
:ipn' cam-ras' ''^*''" *'°'"' '» " snaked to- 
yes acrf,F5 10' "■"■'' '''e f°'"' 
)r at ground 



of the men in the trucks waved ij 
as they passed, like troops go- J 
ing into battle. They appeared! 



in one mi 
time will be H-hour minus two 

Fifty seconds later he coimted 
down — ten, five, four, three, two, 

There followed one of two 
TNT e.vplosions. set off to test 
shock-wave behavior under pre- 
vailing weather conditions. The 
second followed an hour later. 
H-Hoiir Jfiniis 30 .Minutes 
I The voice was silent then and 
desert vastness engulfed the si- 
lence. Half an hour before tar- 
get time it came again through 
the speaker: 

'In 15 seconds the time will 
be H-hour minus 30 minutes." 

Then the count down to zero 
again and the tenseness mount- 
ed. All unnecessary electrical 
equipment, such as automobile 
ignitions, was ordered turned 
off against the possibility of In- 
terfering with delicate electronic 
signals; 

The voice told of the B 50 drop 
plane passipg over the target 
area with two others flying sci- 
entific equipincnt. , Still another 
850 trailed this formation, car- 
rying other Instruments. 

The voice told of mililarv ef- 
fects instrumentation th'ree 



Then the at 

"In 15 seconds the time 
H-hour minus 15 minutes." 

And again the count down to 
zero. Observers hastily checked i 
their watches, fiddled with their I 
cameras or binoculars. Bright! 
sunlight brimmed the ba.sini 
ahead now and the towers, the 
earth lumps of the dugouts, the' 
glistening wings of the tesi-sub-j 
jecled airplanes were easily vis- 1 

I Five minutes later, from tlM 
■control point, an unearthly me- 
chanical ■ scream wailed across 
the desert— the Ifl-minute warn- 
ing siren. As it faded the voice 
returned soberly: 
I. "Observers having four-point- 
'five density goggles should have 
them ready to put on at the 
minus-one-minute w-arning. ' 
Those who do not have them 
should face away from the tar- 



get ; 



;the 



warning until appro.\imately 
plus five seconds." 
'_ Silence. Then the position of 

the drop planeTn the sky. The 
number of seconds between the 
.drop of the bomb and the deto- 
nation. Again the drop-plane po- 
sition. Then: 

I "Minus one miniile. Minus one 
minute. Put on goggles or facei 
away from the target area ... 
I "Minus 30 seconds ... 

"Bombs away!" | 

Observers breathed quicklv in' 
charged air. Through the black ,i 
goggles they stared transfixed' 
toward cround zerrp. They braced 
themselves f.^r violence, anti':;-' 
patiiig the une.vpectcd. 

"Twenty seconds . . 

Now the bomb was falling. 

"Ten seconds . . ." 

Then the aggravating ccunt. 



"Five 



four , 



three . 



176 



rnrnn 



OPERATION TUMBIER-SNAPPER 

RADIOLOGICAL SAFMY 

HEPORT TO TBK TEST DIRKCTOR 

t>r 

PhUip S. Gwynn 
LL Colonel, USAF 



Hcadqaarter*. Arsfd Term 8p«cUi WnpoB* Proy«t 
WmAl^tM Z>. D. C. 






177 



U (tWMir.ATTCTI 

lo order to ecny out Um rvtpenslbllltles uslpsd by tho T*5t 
Stivetor to Mm lUdlole^cal Safelf Croup, Um Rad-S«f« Groip w«i or>- 
.t>nlzAd ks s.'.0vn on Um ere«alutlonal cbarl, Figur* 1.1. This etui^ 
doUasates thr mas of opvrttloiiU. rsspoBslbULltUs for tba Rad-Saf* 
Ctotqi. Tte IsMdltU u«a of tfaoilt«wu U» raspooslbUllr of tba Oi>- 
Slto Cporatloas Dcputaoot. i soeooJ art* eonslattog of ths Urrltory 
•ztcttUat fnn appnnlaaUlr a ZO-olla to 200-ail*. radius froa th* t«3t 
■lU vas tin rvspoRslbUltj of tba Off-SlU OparaUons Dapartaant. la 
addition, a laetloo vaa aatabLUfaad to eporata froa Indlas Sprlsfs llr 
Forea Base la ecajtsKtioB with tba oparatloos of tba Special Vaapocs 
Cantor. 1 fourtb saetloa vaa ebarc»d with rvBlablac ^^ loflstleal 
for tba Baid-Safa Cronp. 



1.3 HXjOII.SJJ. 

Tba Rad-SaTe Croup vaa eea^oacd of persoimel fr«B tba Drparteeata 
at Anqr, larr aad Air roree, aa foUova: 

(1) 2l6tb Cbesleal Scrrlee Coivaar, eonaUtlag of four offlccra 
aad 13% enlUt«d sen, fraa tba Rock7 Mrait&la Araeaal. 

(2) 17tb ens (Cbsleal Tecbaleal lBt«lll(csee Detadont), con- 
•Utlac at tvo orriccra aad aerca oilljtcd aea, froa tbe Any Cbflral 
Center. KarrLaad. 

(3) 99;tb Qurtesata* Uandry Cot^uvy Drtaetaaeat, eanaiatlai of 
on* officer aad 1% cclljtcd acn, frOH rx. Oareaa, Kaaaacbuaatt* . 

(h) riTv officer* aad flra caUatcd Ma froi tba Dcpwtarst of tba 



(5) Ta efflecrt frca the D ej e itn o i t of Air roree. (Itaa rotated 
aftar cptrastaatelr %} <a7« «ltb Blaa other V3Jt efrieers.) 

(6) rire offlcen froa Icadqnartcxw, ATSVP. VaaklactOB, B. C. 

(7) Tteec offlcen aad arrca cnlUted aea fttai Test Ci,— nil, tfSVr 

l.J.X Pre-teat RM-6afe Tralalag 

A aeetlac attcaded by aU tbe Rad-Oaf • off Leer* prraant at 
^be alt« vaa held on 17 nareb 1992 to detenilse tba baekcrooid, 
.aqpenoiee nd eepebUltU* of the pcrveml of tba laA-eafa Oroop. 
Slaea only a »«rr fev of ' 
opine Im cr parttetparted la ndlaleclcal aafatr aort. 



178 



' (1) Or(ul:atlao of tbe Ra4<Sftft Cnius 

?^<|M/Ulblll*.l«9 

Cpenttoaal rroc»4\3«i 
Supply Preea<:ur*9 
Smtrjrltj Kaasursa 

(2) Ccwnl Sa<i-5«r. rrlnelrl^s 
Kadlctl iipsets 
RciUttloB Tolcnac* Ualti 
Pcrtoaasl D«ooat^aAa*.tao > 



(J) iUdlte Inatnannt] 

Prlaclplai or C^ntlon at tia tiS tai KI-5 Ii>- 

atncaDts 
C«llbr*tloo Metbodi 
35« of In«tr^nt« far riold KonltorlB; Sarrr/a. 

(NoUt Um of rsdlBS lBjin«»nts for Mrl*! 

■oDltorlBg voa eoTtrad jtp&ratolj b^ tha Off- 

SlU Oporttloiu DtiMU-wioet for doalpiaUd iadl- 

rldunlj of this Capu-tnet.) 
CftUbratlea of Inatnaao'.s by £«eb IndlTlihal 

U) 'ioUlarlxatloB TrulAinc 

Rui-Safa Building ard raeaitlas at CP 
T«9t SiU m» rotUlarUatloa 
Prograr aad Projaet Hoiitorlug 
Praetlca Surrays of JiXlZ Area 

This tr n'T'r c projTBi bcpui oo 20 MAreb asd ee?tl.iu»d to ttw first ahot 
DO 1 April. r-.=-tbsr ^:en^ trainloe waa also cdaductaU la tb< tv>-w«ak 
Ictcrral b«tv«ac tte first aad saeaad shots. iDdinduiU oc>-'-i»>Job 
tra lnlr g was e:oduet«d tbreugbeut tha rrnalr.Ur of t>» op^ratloa. 

1.4 r.'USCT ACTirmss or thk m>-sajt crq-? 

1.4.1 Utl.tan vlth :}» X«* Tort O'^rtV.rn. Cffl« 

Tbe ar»a atartlJM approzlsatclr ?» ellca feam tb- test »lt« 
vos cOTcrcd b7 inro. Drpecdja« upoa tb* visd prcdletlona oa £bot Cay 
cljru 1, ti« r«prat»nt»;iT» of tb« KTOO, Dr. ."^rrtl ». Els-isbud, aad 
tha Off-Slta ?.ad-Safa CVaratloas Cfflear posltloond ■oaltarlae tws so 
ts to braeicat tb* pradletad faXl-«ut araa. Tba XTOO socTvd rroa tb* 
Crr-SlU Offlco tba actual elood trajactarr data obt&l.-»d ty tbo aerial 
terrala (array ta^s, aad asad tMs laforaatisa to pcsltlea tbnlr air 
• lopllaS ttatleas. ttest of tba dlfflralt public ralatlcas prableaa 
arosa frca en— nitlas jraatar tbaa 300 >llta trza th« iite. Cloes llaii 
wltb tbs K700 Bada safflelaat laforBattna aTallabl* ao tbAt Uir;ulrl>a 
ftea apprabaaslra eoanwatlas could ba anavTart vltb eartalstj. 



179 



X.*.r ClrU Acrooautles AteUU'.ri-.tlcr. Ll^^lBtn 

!.l«l=oa voj eAlnlMaC'I -/".Ui the CU. r«jreient»tlT«, K.-. 
CrMnlcaf , tsrou^bout the operation to Inaurj safety for -ossereltl end 
oth'r aircr»rt Hylafi la tho Tlelaltr of «><• test .Ite. Tbe Off -Site 
Office proTliiird InforoBtloa to the CAA rcpreieotatlre vileh vaj •jjti to 
dctcraloe th- aeeuraey of the Hrvmrs closure forecMt Bade 9a «tot da? 
Blaiu one. ThU Infon^tlon helped reduce the cloaure tloe for al.-/BjB. 
The radio net aTallahle to the CAA v« extreaeir Tt*\>ahl» on tvo of the 
shots, vten the traekla^ aircraft lost eoataei vlth the site. To* 
position of the cloud oad other aUled data wra then r«l»r;i throu^ 
CAA statlou. 

l.k.3 Liaison vlth Dfsert Roct 

Llaljon v«a nalnUlJied vlth Desert Roeh Operation* tj at- 
taehlBg sa officer fro* the Bad-Safe Croop to Car? Desert Foci as a 
technical adrlror. In accordance vlth Rerad* ProTla« Groimda Rad-Cofs 
policies, tha —'<-"' pcralsslble eiposvre lerels for personnel a=d 
tolerance lertls for rehtdcs, etc., were estahllsbed for Desert ?.oei 
la a letter to tbe Teat Ceawiad. The Rad-3af« Croup furnished Opsratloa 
Desert Rock vith flln badges and processed sa»e. Alaa a snail rJSier 0. 
faJIae laatnaenu and doslaeters vrre loaned to Desert Rock. On Chots 
3, U, and 6 the Desert Rock surrer noaltors aade tie Initial surrer vlth 
the BMltors fron tbo nad.5afe Croup. On Shot 7 the Desert Iloek 
Operatlen nno called for an laoedlate advance foUavl»« the detonation, 
and the laltlal surreylan vork U their area vma aecocpllsbed br Desert 
Rock Rod^Safe personnel. Since the safety of a large mober of par- 
ticipating solitary persotmel depends upon a cccpieie naiiirstaadlE^ of 
the potential radiological hutards and the proper utUtxatloa of physical 
data, snch aa veather conditions, vlads, etc., a tlja was estahllahed 
baaed upon as eralnatlon of these pertinent factors at vhlch the troop 
participation pperatlou for each shot vtiuld begla. Once thU ttoe had 
been eetabllshed, the responjslbUlty for aeeospllahlag the exercise In 
eOBfcsiaac* vlth tha cstabllatv.d Rad-Safa policies vaa assiaed by tha 
<•.— — <t-j ccoeral, Casv Desert Rock. 

l.k.k Unison vlth Proeia 22 - 'SoU Analy iU and raU-out 
Studlea " ~ 

Progrsjs 22, headed by Or. Kermlt Larsea, UXA, vm« a r «- 
seareta ptop" *« study tha rheaosieiiology of radloactlre fall-out frm 
an atOBle explosloo and the co<vo«ltlon of the soU at tha test site. 
SlJics this progr™ and the fall-o«t ■cnltorlng eoodnrted by tha RaJ- 
Safe Croup had>>lBta of vtoal Uite«at, tha data o6t*lMd by both vaa 
fteely cxehangad. Tha Xad.««fs radlA oat and tha C<»mtlr« Uhorvtory 
Mrs shareA by both ariwn1fsM«wa. 



180 



ill 






m 



nil 









a fi^ m >^i- 



jl 



ifif 






-01 



181 



T.V aljilc.-. of -.hf. Cn-ZHo C7>-r«t.lo»s 0»?irL»;ci vas ti l=r:<'=«=t 
•■^.f policies, i'.Ttf.ivDs uui cT-iiri of '.he 3ir«e'.o.- of ihe ?.«i-b-..'» 
Cre,;? Vs acccspllsh Um roUo-Jln,- objoctivoa uUhln the t*rE<r. ilto*, 
lncludtr< l!«reuiy; 

(1) HoniV:r:ni of ridlologlcili? conteainaUd arees. 

(2) D»Un*»*.lon of rndlolocl^iUr csn'-iolratcd areas ty 
field j-ineys, di.«jrf=:ln£ ;aia bj- saps, oT^rla/s ar,d '.aVuloUd re- 
?or*.5, acd soatlsg apprsprlat* jlcnj to iirfleata th» 10 =r/hr, 100 
nr/hr, 1 r/hr ar^ 10 r/!ir IsolnUrjl'.y IXnea in the target area. 

(3) Briefing of taehnle*! roeovorjr perjonocl oa tio e-.=?«3t 
radiological sltuAtlsn in the tarpst areaj poat-ihot prior to tialr 
entry Into thej"? areas. 

/ 
(i) Monitorlrg a-nd l.isuri.-^ proper deeoataalnatlon of per- 
sonnel ret-.irnl.ng frca eocta^cated areas. 

C5) :<cnitorlsj asd deconUsinatlon of nhielos ead recoTery 
equlrze-t r* •-urr.iig fr;r ccnt<i-lrated areas. 

(4) rrovldl=g teat per;oc.-»l with dojlaotera nad fil= 1 1 
hr.ii;es, pTzenz'.-z esi l.-.t«rpretlcg the dosape readlAjs, axal asilig I 
pcmux.-.t recjrdj of tr^rse data. .' | 



The cr|,vu;3tlcn sf li Or>-31t» OperiMois Departar-nt 1; ;hc."o Is 
t>.o CrEi.-.i:atlc.-.al Chirt, :1.;. 1.1. This Cepirtaoat oce\:pied f.-A 
;:;ili:«i tho aijor purx, of tee fiad-Sife DulLdLng. Tbo Laltlal Officer , 
It Chirip of '.his Oepirtscnt vao Lt Coloaol L. E. TV.-py>n, vto w&a ( 
rtpliced i-/ L". CoIo.toI ?«-il C. Day ca 3 Kay 1752 for ts» rrTainder ai i 



osj Officer's ^jrstloas vera aj follows? 

(1) 0-«rell rjpnrrlslon, ilreellos aod control of aetl 
ties pemlaant to Ca-Slte Cperatlosj. 

(2) AsslgmBnt of perjonoal to jpeclflo duties within 
L«part»iit. 

Jl 



182 



(3) Coordlno'.lnc ihrwich tf« pncrno o^allnrt vJVh tbe ;.-?- 
cms le/itlrr.r l/j del/jralm? Ihe (milelp»i<d ?.«4-0«r» r-7ilrra»nts of •->/• 
rceovory rnrtlas of lh» various pniie'.a • jilcrfd to collect >chru' *1 
•laU. 

(4) *::l(7c»nl of P.ti-CsS' so.iiVers *.5 •ceoc^'UT' t«chaie'.l 
rreoTcry /Lid field vorlcinc pu^lo: i3to tJM costtaliMtMd «r«*i. 

(5) Privid^ flc*l ?.«^:kf« elairux* for Tteartrr *rA v::t 
p&rtie: Ijito thess trrns. 

i.i Pir7Ti:.r, At.i Kip-.-nr. stttoh 

Tho PlollLnj uid Orlcfloe R«eo sar-ni 43 *.h<» Ir^orsitlon e«nUr 
for all oi>-:lU field oparatloaj. It was '.bM^fucetlon of Um FloV.l.-^ 
acd Briefing Section tot 

(1) S'rlef tho Initial >3st»-ihot nimy Uaj aad prepar* ti« 
ba:e cap of thn tarc»t areas, ladlcatln^ tbe locations of p«rtliwnt 
test data coUaetln^ statlocs, and the pcisoiMnt access reads, as v«ll 
as tbs elcht radial 1L»S of r-.r-Stred voodoa staxas eestarad on (rsu::d 
zaro aod oriented toward the el^t principal points of th* eec^ass. 

(2) Ree«lTe froa the post— s>wt Ir^tlal surrey tvaas by 
radio their reMrts en tho locatloM of tb* 10 sr/hr, 100 sr/kr, 1 
r/tr aM 10 r/hr and/or cro«i»l »«ro readings, with raferfae* to th» 
nruered atiJcos. 

(l) T-.VJ.i'-ft ty« r»ailrv:s rfe<'lv»<; fr53 tV rJr-.xy t«a=s 
n-id -mo '.■■^;- int.1 to .-"lot and doUnaata oa nap oTarla/a th« radlo- 
dCtlTii Isolnlcni'ly Unas. 

(i) !Tl«f vrA Ksslcr. t>*> ?.a4-3<if« e-'^iek point p«r»oaiol tc 
th^lr deslp-ji'.nd pcs'.s. 

(5) "rlef all Uihnleal rccprery pirtles and their ajslj^j-J 
Vjl-3afe n-iratcr.-i pr> the mirreot r/wllolcclcal aituAtlon le the tarjot 
areas prior to t:-^l.- departupt Into the field. 

(••) rrtpare for aubalasloa to Vj> Olrretor ef tho Had-Pafe 
CroL-p arJ to ^he Off — Slt» Operatleaj Officer dally ta^ilatei rerartj 
aM -MP averlryr alowlnc the e^imint radlelcglcal cents^nat'.oo larelj 
In the teat aiva. 

(7) Dle7«tch aal ecntrol all rahlclea aialc»d ^ '-^ C»- 

31U Cyrratlcrj Departaar.t. 



183 



(1) )■«?,: lorlnj of i\U p»PMrj»>l rr'.arr.tnc Vi v:/> RcJ-CiTt 
tillll.-.!; fr'is ecr.te=ln3t»d np-nj, and Ir.rjrlng ih.V. U.9:«i vf.h l»vol; 
ef rsiljn;*.!-.-* c?r.'-;a:rji*.lon cbov? ih« establlahad llal'.s perCorsni 
;er::.vil d?ecr.lii=in.illon. 

(2) Insurlaj *.h«4 oU. ceat^nat«d protectir* clotiis< vnj 
pnr-rljf ••uTMi Is to •-!:« P.ii-S*r» Simply ftTietiaal ttf.'.orjti la vJi* 
"srisi-il Secer.ta. -i' n ation Jlrtt for thl» puipo:*. 

(2) ?-e-oo.niVjrlr.g of Ui Indlrldads, »f'.#r a.^wsrln;; «/l 
2:r^bb'..-.(; dceontooloAtlon, to ituurt that all traces of cectoBlesttca 
ba£ b>en resoTad. 

This Section op«r«Ud In » EP4e<iLll7 pnparad a.->»a J«st east of 
th* .^ad-S&fa Building and perfoTStd e» foUowiae fuzctlons: 

(1) Konltorlng of tU va.Mclas and r9C0Ter>^ ex^'.raer.l cad 
zst^rlfl brc;:jht to the Oecostaalnatlon Station froa eonticilr-ited ertas. 

(2) Detoolloa for d«esnt>ialnatien or naturai d^eoy of ill 
such vehielei aad eqvlpaent Indleatlnf IV-easltlos hlctwr thon 2 i.-,'hr, 
S^=« oaly, as p»»d by an KI-5 C«lj«p-«»Uer Cou=t<»r vlti tho r".-<> 
held npproxlaatoljr i, to u Inciirs fraa USo surfaces b*l.-.i; :or.ltar%d. 

(j) DrcTaVAilnatlon, «s refilred icyj feasible, of vehtclis 
a=d »-\i:;=i-.-.t >i^:/» tel»rifl':e Uvi«ls aft<>r Taeisia clea-Tlrc b.-us-Mw:, 
w«:M.V wl'..'. cl'W w«'^r, hot water wid det<ire«al, er with Mch pror- 
riTt s'.'tes tad I'.c'.er.r'Bt. 

;»/ r.'ln^* •.' «y.:j5r:i»>l parties of t'KIcIos «."v1 "iiiiyoool 
.-;v;ri;r-^l'./ i-rsnt.-.'iir-itei *.o l^low-'-olorcjtca lernls, a=d dwten'.ioa 
f:r TK.i:-'.-.::-:') -leetx of ttose rat recpondiog to the abore deccataali*- 
•-Icr. ;re:ci-jj>os. 

(5) Sclc^it fcr reaoval fras tho Cr Area, upon direction of 
•.y.~. rLrc.-".:r, r.r..'.-Cjf« Cro;5>. cf t-Mc1o» aad reeo»ery e^ttipaect stUl 
-.i-y/t t^lrrM.:* Irrrlj when rpee*. fieallr rn^ested by the Director of 
K^ltir;.- iff'tcts Test Cr:-.^ or '■'•,pons SeTelopeast Test Croup. 



mar ta the be^.c-Mng of Pperatlon ZrySU-^SiXTTZ^. Th- F-ai-Cife 
:j7 v«j serrtclag daily a nr'r-i of 112 peraos vbo vere »r.f«i:»<! ia 
e fiaal ;hav«s of Cperalloa JiSlir. Ourla^ this tl«» flla t»do»» '•"^ 
ppllol by t.\» Health 3lTlaloo of laa J^^aw* and were iwUimad there 

33 



184 



for r'<>J"S"'-C' I" ^*^ lilt'r par*, ef Kveh ts? y>i3Vts?«;B".; 7roTtj»- 

h«lp of yj-. vilH«a Di;.U»- frsa Loi A1«30S. frse th»t •-!»? un*.;l '-iw 
eonelualon of '-"ic TVraUa-OWJTia Or«.-«'.lon tAJt 6»<;iJon, eSMl»t:=s 
of orw? officer «i.i<l l8 tnllstetl a^n, ynern'ri all flla V«l5Ti for kU 
Irs*. r«rtieirv)lB, tncludlnf Cts? BM.er*. Rxk »ai th» offtclkl »ni 
trermlcal ohscrrrri' pro^osi. Tio virkln-: tbtftx wre »*: 'if, cr.< 
ercw worklM, on the <ay :Wfl, y-.e ovhrr ercv iM'.cj; orer ".bT n'.cii 
•hl.'t, to per.'or= tk- vork o.' tfclc Sr;ilon. Ti;; 50^000 eonT-nf.".»l 
flls baC:»3 Inf.lallr pro-ured for -.he rJXrUS-CrJl??!? Operatic: tJ-- 
rl»cd by 15 KAreb. An sildltloo*! 15, COO such flla \)*£*fi* pr^rurei 
«rter '.t* f-Art of 'fee TWCLO-SlUPTja C?-ra;loo arrlTed at SK li 
April. FJla baigea vrnt calibrated aM proceaied by atA»!ard t«c^.- 
nlquea <Ully and Bade armllable by C&JO bo-ors tie following day to pro- 
Tide the Director of Rad-£ar< vttb the cus^atlre doaagca prior tc tb« 
rc-ertry of peraooi Into a cestaalcated area. 

rau ScctlOB perforM^ t.>i« foLlovla* fvjactloni; 

(1) Proe-jrloe froo tSe Rad-SaTe Cjpply Officer for re-:«iu« 
to authorized teat perfOSDcl doalaetera of rvrlouj raagea and file 



(8) rroper calibration of doalaerera, cbarKlr.« tSeae dc*l- 
eeter* to lero reading prior to Isaue, and readlsc and rceardlii< tbe 
Indicated docagea upon their retura to tbe Doilaetry Sectloa. 

Vi) ProcenlBg of all Rad-Safe flla bM!«e« vjm tbelr re- 
turn to the Ooalaetry Section, reading their optical dcnsltte: by 
oeana of properlj adjuated photo denaltoneten, asd eonrertlzg these 
optical denaltlea to dote readlngi froa pre i loua ly prepared eallbra- 
ttOB ebnrta. A prrsonnt record of th*ae dosage readlsga vaa ca«r 
KgalDat thr lodlTlduolc e^t and oroiniutloo. 

(k) Dally prcpnmtJco, for suValeitoa to tbe Director cf tto 
!t&d-£arr Croup, of lotegrated deface rrporta fbovln;; each lallTl 4.al ' • 
Cicx, (Tndc and organ^iatloa, and iDdlcatlsg by red underaeore aJi^ 
IcdlTtduala wte bad cixeedcd a total Irtrcrated doae of 2 r. 

V.8 OtTyATIOTo 

Tix Kcr.cnil oreratlerja rr«'dor*a felloveJ by the Cn-Slt- Sfran- 
srr.t th3-ouf>Jut tV TV3ta»-SSAPrES Teat Series vaa ^^tabll^^ed Ir. tie 
3tM<il6£ OpCTatlEC rroeedure for the Ca-3lte ?ep«rttcnt. For tbe rir»t 
four shot« tbe ?o€lr»trT and Recorix Section va» under the ruTerrliloa 
rf the IxnUtlca and Supply Orp^rtnent, and rer th« lajt focr •hoti 
thla rectlca v« placed m>d«r the direction of the On-Slte Det».!_-=t. 
The SCP oentler.el abore vaa oraded J Kay 1952 to r«n»ct thla cbaige 
of reapoaalbUtty. Acfjal C7«ratma perfemad by th« TWlooa aertloca 



185 



•.t '.\7 >..a.*.T >;irv.K".t »rr ?*vrrH by ;b« •■>vtr.l;e?s for t^s s>/»t 
.••.r cJr.Tr.-.tc.-.j« tn lor^iJ-r'.rj; •.fcr ;r?>sliet ^Ixv.lrjc u.i ?r»>».-ai:oB 
fir •.."•.•; 5Mt d«y e;?r«*.:ena v.* ts? fjb3?iuent ^ftf.'.'^ai ^f.^r wei 
shot &17. v-t •Tpfr.l'.:?] ecr«r tf.f reUovir4 p«rle-U of tts«: 

Ar;ts:jx A: 27 Kires (/Ot-l D<»r) *•» 1* April (B-I D«y/ W2 

*rr^.-.l«.x B: lU A;rU (?-l Zny) 'o 21 April (C-1 D^r) 1752 

A;;-ailx C: a A^:l (C-1 Cny) u> 30 AprU (0-1 I>»y) 1952 

Art-r.dlx 3: 30 A;rll O-l Zay) -.o 6 Kay (E-l C»y) 1952 

Afftzilx Z: 6 Kay (£-1 Zsy) to 2k Kay (P.l Day) 19J2 

Ap7r3dlx F: 2k Kay (r-1 Say) to 21 .Yay (C'l Day) 1952 

A;?e:<liJt C: 31 K'r (C-1 3ay) to fc June (B-1 Soy) 1952 

A;peodlx H: k Juec (3-1 Bay) to 9 Jim (B»3 Cay*) 1952 



186 



ONA 6021F 

SHOTS 

EASY, FOX, GEORGE, 

Ar^D HOW 

The Final Tests of the 

TUMBLER-SNAPPER Series 

7 IVIAY - 5 JUrJE 1^2 




^ 



OEC 1 '.S32 j 



United States Atmospheric Nuclear Weapons Tests 
Nudear Test Personnel Review 



i.'.i! doc-rat-t has }o«. 
f.-: DubHc te!e<i:e c.-.d ile: 



by t^.a D-'efiso Nuclaar Agency n ExocutJv« A g*»nc f 
for the Departmsnt of Defense 



187 



Aerial Surveys of Terrain 

After the detonation, two C-47s and one L-20. based at 
Indian Springs AFB, conducted radiological surveys of the onsite 
and offsite terrain. One C-47 (tail number 386) left at 0530 
hours, flew at heights of 700 to 5,000 feet, and returned at 1200 
hours. The other C-47 (tail number 308) left at 0715 hours, 
conducted its survey at an altitude of 10,000 feet, and returned 
at 1230 hours. The L-20 (tail number 464) left at an undesig- 
nated time, conducted its survey at 1,000 to 7,500 feet above the 
terrain, and landed at an unreported time (1-3; 36; 37; 52; 69). 



2.3 RADIATION PROTECTION AT SHOT 2ASY 

Tt.e main purpose of the radiation protection procedures 
developed by the test groups and AFSWC for Operation TUMBLER- 
SNAPPER was to keep individual exposures to ionizing radiation to 
a mini(num, while still allowing participants to accomplish their 
missions. 

Logistics and Materiel 

During the period 7 May to 24 May 1952, which covered the 
7 May detonation of Shot EASY, the Logistics and Materiel Depart- 
ment issued about 525 film badges to test group personnel (both 
DOD and AEC personnel are included in this group). The depart- 
ment also issued 1,174 sets of protective clothing and 253 
radiation survey instruments (43). 

Monitoring 

The initial ground raoiation survey began at 0522 hours, 
slightly more than an hour after the detonation, and continued 
until 0650 hours. Because of the relatively large radiation area 
and f.ie rough terrain, it was not possible to complete the 
survey, as indicated in figure 2-3. The closest that the initial 



188 



The Desert Rock Radiological Safety Group implemented 
radiological safety procedures and was assisted by the 4FSWP 
Radiological Safety Group in radiation surveys. Eieh survty tea.n 
consisted of one driver, or«» radio operator, and one radiological 
safety monitor from the Radiological Safety Group. An AFSWP 
radiological safety team accompanied Companies A, B, C, and D of 
the 701st Armored Iiifantry Battalicn into the forward area. The 
70ist provided additional radiological monitoring for its units 
tnat went into the shot area (49; 51; 53). 

The Instructor Group consisted of AFSWP personnel who 
replaced the less experienced Army personnel used at Shot.<; 
CHARLIE and DOG. After the detonation, the instructors led 
observers through the display area to view the damage. They 
noted differences between the predicted and actual effects of the 
burst (51). 

In addition to the Instructor Group and the Desert Rock 
Radiological Safety Group, several other Desert Rock support 
elements participat.;d in activities at Shot FOX. 

R*?fore the shot, personnel from the 369th Engineer 
Amphibious Support Regiment spent several days in the equipment 
display area placing military vehicles and ordnance at various 
distances from ground zero. Observers compared the preshot and 
postshot condition of these displays (49; 51). 

The 31st and 23rd Transportation Truck Companies transported 
"•ilitary personnel to and from the forwaro ares. At shot-tim*», 
the vehicles were parked about 1,000 meters south of the observe 
trenches (49; 51). 

The Desert Rock Signal Detachment established wire and radio 
communications within the forward arei, as well as at Camp Desert 
Sock. After the shoe, signal personnel operated tn<» t*o moMle 



189 



Monitoring 

Following the detonation, D-^sert Rock monitors surveyed the 
approach route to the equipment display area. These monitors, 
unaccompanied by AFSWP monitors, noted radiation intensities 
along the route and located and marked the 0.5 R/h line, the 
forward lijnit for troops. After the monitors had surveyed the 
display route and AFSWP monitors had completed the survey of the 
rest of the shot area, the Test Manager declared the area saie to 
enter. Desert Rock monitors accompanied the troopw as they moved 
up to and through the equipment display area (49; 51). 

D econta-Tiinat ion 

Personnel were brushed with brooms to -remove contaminated 
dust when they returned from the trench area. Monitors then 
checked all personnel with AN/PDR-TIB meters. Those individuals 
whose readings could not be reduced to less than 0.01 R/h were 
ordered to the decontamination station at Yucca Pass to shower 
and change into clean clothing. Monitors checked these 
individuals after they had showered to ensure that intensities 
-n their skin were less than 0.0015 R/h {49; 51). 

Vehicles were ilso monitored and sent to the decontamination 
station if brushing could not reduce their level of contamination 
to less than O.Oi R/h (49; 51). 



3.3.2 Joint AFC-DOD Radiation Protection Activities 

Information on Shot FOX has been obtained from the radiolog- 
ical safety report prepared by AFSWP (43). Tt.e document includes 
data on radiological safety equipinent. onsite and offsite 
monitoring procedures, and radiation i.= ;»in tensi ty contour maps. 



DA/Al^^>^^ 



83-529 95-7 



190 



Logistics and Materiel 

During the period 25 through 31 May 1952, which covers the 
25 May detonation of Shot FOX. the Logistics and Materiel 

Department issued film badges to about 340 AEC and DOD personnel 

involved in test group activities. The department also issued 

549 sets of protective clothing and 260 radiation survey meters 
(43). 

Monitoring 

Initial ground survey monitors began recording radiation 
intensities at 0512 hours, slightly more than one hour after the 
detonation. They continued their survey until 0645 hours, 
approaching as close as 460 meters north of ground zero, where 
the radiation intensity was 10.0 R/h. Initial survey monitors, 
however, could not survey the area to the northeast of ground 
zero because of radiation levels in excess of 10.0 R/h. Monitofs 
conducted resurveys on subsequent days. Part of the FOX 
radiation overlapped the residual radiation from Shot EASY, as 
indicated by the rP-^iation contours to the south-southeast of 
ground zero f 43 ) . 

Significant fallout also occurred northeast of the NPG , 
particularly in the area of Groom Mine, Nevada, about 30 
kilometers from ground ::ero. where the highest recorded intensity 
was 0.32 R'h, seven hours after the detonation. 

Eight to 13 two-man mobile teams participated in the offsit*^ 
monitoring. Abour six hours before the detonation, they loft the 
test area for assigned offsite locations. 

In addition to the ground survey teams, two C-47s and t»o 
L-20s conducted offsite surveys of the terrain. The C-47 
aircraft ntT.sured radiation .nrensiti'^s of up to 0.03 •! / h 
approxirTijit.'l y 75 k i i omt' ter.s nor-heast of gr'->urid Z'^r.-^. Tt:" 
h)gh*»<;t radiari-^n intensity pii -riiir. ter^'i by th--- l.-2i;-'. las 
0.0025 R/r, , 4j 1 . 



DMA (^oi\ ^ 



191 



^yice^^?^ 



U.S. Department of Commerce 
National Technical Information Service 



lllilllillllllllili 
ADA 122 242 



OPERATION TUMBLER-SNAPPER 1952 



JRB ASSOCIATES 
MCLEAN, VA 



JUN82 



192 



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193 



OREGON 




Nevada Proving Ground 



Figure 1-1: LOCATION OF NEVADA PROVING GROUND 



194 



HOW 

FOX 

EASY 



10 

I 11,111 

Kilometers 




Camp Mercury 



Camp Desert Rock 



Figure 1-2: GROUND ZEROS FOR OPERATION TUMBLER-SNAPPER 
AT THE NEVADA PROVING GROUND 



32 



195 



coordinated all activities of the Radiological Safety Group and 
informed the Test Director of onsite and offsite radiological 
conditions. The Radiation Safety Director was also responsible 
for radiological safety operations at Indian Springs AFB 
(91; 134). 

The following elements made up the AFSWP. Radiological Safety 
Group (53; 91): 

• 216th Chemical Service Company, consisting of four offi- 
cers and 134 enlisted men from Rocky Mountain Arsenal, 
Colorado 

• 995th Quartermaster Laundry Company Detachment, involving 
one officer and 14 enlisted men from Fort Devens, 
Massachusetts 

• 17th Chemical Technical Intelligence Detachment, con- 
sisting of two officers and seven enlisted men from the 
Army Chemical Center, Maryland 

• Five officers and five enlisted men from the Department — ~ 
of the Navy 

• Ten officers from the Department of the Air Force 

• Three officers and seven enlisted men from Test Command, 
AFSWP 

• Five officers from Headquarters, AFSWP. 



The activities performed by the AFSWP Radiological Safety 
Group included (91) : 

• Advising the Test Director on measures to ensure the 
radiological safety of all personnel involved in the 
operation 

• Furnishing all ground monitoring services for both sci- 
entific programs and radiological safety procedures 
within a 320-kilometer radius of the NPG 

• Providing current radiological situation charts and maps 
showing onsite and offsite data obtained by ground and 
aerial surveys of the terrain 

• Issuing, processing, and maintaining records of all 
personnel dosimeters 



AOA 



a^->4> 



9 



196 



6.3.2 Instances of Gamma Exposure Exceeding Established Limits 

As stated in chapter 5, the gamma exposure limit for 
participants at TUMBLER-SNAPPER was 3.0 roentgens (108). Cloud 
sampling pilots, however, were authorized to receive exposures up 
to 3.9 roentgens (82). Table 6-7 lists the units or organiza- 
tions that included AEC-DOD personnel who received gamma 
exposures in excess of the established limits (22; 72; 142). 

Several of the overexposed personnel listed in table 6-7 ' 
participated in Military Effects Test Group projects that ^ 
'required them to enter radiation areas to retrieve instruments 



and record s. Some of these projects , witn tneir iielding 
organizations, are : 

• Project 2.1 (Signal Corps Engineering Laboratories) 

• Project 6.1 (Bureau of Ships; Signal Corps 
Engineering Laboratories) 

• Project 17.1 (Los Alamos Scientific Laboratory). 

In addition, research indicates that the individual from the Army 
Chemical Center participated . in Project 1.9, "Pre-shock Dust," 
and that the participant from the Engineer Research and 
Development Laboratories took part in Project 3.4, "Minefield 
Clearance." 

. Overexposures resulted from a variety of activities. For 
example, most personnel entered the test area at recovery nour or 
when permitt ed by the Test Manager, but personnel from Projects. 
1.9, 2.1, and 17.1 were permitted to enter the shot area before 
recovery hour because immediate recovery of equipment or data was 
necessary to ensure accurate results. Personnel from Project 3.4 
inspected, recovered, and replaced land mines that had been 
placed around ground zero before the shot. To complete these 



' activities, personnel may have spent considerable time in 

(radiation areas. Project 6.1 personnel tested various radiac 
instruments and survey techniques under field conditions, which 



197 



required them to enter radiation areas (22; 46; 72; 92; 116; 138; 
142; 143; 151). 

Members of the Radiological Safety Group provided 
radiological safety monitors for all shots. These monitors 
accompanied AFSWP project personnel on many of the recovery 
missions. In addition, radiological safety personnel surveyed 
the shot area after each detonation and manned the checkpoints to 
the radiation areas. Members of the Radiological Safety Group 
spent more time in or near radiation areas than other personnel, 
especially because they repeated their activities during several 
shots. Personnel from the following units were members of the 
Radiological Safety Group at TUMBLER-SNAPPER (91): 

• AFSWP Test Command 

• Carswell AFB, Texas 

• Naval Air Station, North Island, California 

• 216th Chemical Service Company. 

The 4925th TeS't Group gathered radioactive samples from 
the clouds resulting from the detonations for analysis by 
personnel from various test projects. Because this task required 
the pilots to fly near or through the clouds, their potential 
exposures were increased (82; 88). 

Documentation of the activities of the representatives from 
the Headquarters of the Armed Forces Special Weapons Project, 
Fort Belvoir, Fort McClellan, Indian Springs AFB, and the 1009th 
Special Weapons Squadron was not found. 






\^^V 



v--" 



198 



si 





a 




2 


a 

s 


, . o . . 


5 




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S 


V 


s ^ - B i 


S 


liil 

< O £ 


^ i i ? s 


i 


Jill 


s S « ? § 


i 


HI 

lis 


1786 
493 

1980 
416 
389 


i 


1 


Army 
Navy 

Marine Corps 
Air Force 


< 

5 



199 



Table 6-2: DISTRIBUTION OF GAMMA RADIATION EXPOSURES 
ARMY PERSONNEL AND AFFILIATES, OPERATION 
TUMBLER-SNAPPER 



Unin 


Plfsonnel 
Idtntified 
by Nam* 


PtrsonntI 

by Htm, and 
by Film B.d9. 


A..r.g. 

Gamm. 

E.poaor. 

IRo.nl9>n.l 


G.mm.€ 


posur* IRoentganil 




<,, 


MO 


1l>3 


30-SO 


5.0- 


Ant.aircialt Aitilltr/ 0»I»e(ini«nl (Proviuonall 


n 
















Arm, Chem«l Ctnltf 


3 




2483 














OeMit Rock IV 


729 


729 


0.153 


288 


432 








Ed9«.0O<,A,s.n3l 


3 




1 949 
















' 




5 930 














fort Belvo.. VA 


13 


12 


3 327 


1 


2 








fort McCiellan, AL 


4 




4613 














fort Mor>moulh, NJ 


3 




2 641 


° 











Observers 


10 




024 


' 











BatJiaiiOr. Safety 


1 




3440 













Sr.lh Armv 


M 
















Srxih Ar-ny Soecal freM Chem.cal. RaOiOlogrcal 
ar^a S.oiogrcal School 


" 


















24 
















ISI Ar-Tiorea D.y.sron. 701 SI Armored Inlanlry 
Batlallor^ 


54 
















nihA„bo.rie0.v,s.on 


13 
















16lhS.9r»IOoe<aiiOn5 8attalior> 


13 

















Atterbury, IN 


16 
















47tn lr,lantr, O.v.s.on 


25 
















82na A.'Borrie 0.».S.On 


96 
















216tn Chemrcal Serv.ce ComMr>y 


" 




1840 


5 


15 


42 


10 


2 


369m Er^g.neer Amph.b.ous SuoDori Regrmeni 


57 




157 
















Other - 


a09 




195 










° 





Ur,„Ur,.nowr,•• 


.26 




165 















TOTAL 


1786 


843 


396 


295 


463 


61 


., 


' 



200 



Table 6-7: FILM BADGE READINGS EXCEEDING ESTABLISHED 

LIMITS FOR DOD PARTICIPANTS AT TUMBLER-SNAPPER 



Unit or Organization 


Number of 
Personnel 


Total Exposures 
IRoentgensI 


Armed Forces Special Weapons Proiect 




32 


Armed Forces Special Weapons Proieci 
Test Command 


' 


3 0, 3 0. 3.1.3 7. 4 2. .17 6 1 


Army Chemical Center 




33 


Carswell AFB, TX 




45 


Engineer Research and Development 
Laboratories 




59 


Fort eelvoir. VA 




3 5.36 37 48.55.6.9.70 


Fort McClellan, AL 




3 2, 10 8 


Indian Springs AFB. NV 




3 2.35 


Naval Air Station. North Island, CA 




42 


Project 2.1 (Signal Corps Engineering 
Laboratories) 




3 7.39 


Project 6.1 iBureau ol Ships; Signal Corps 
Engineering Laboratories! • 




3.1 


Protect 7.4 11009th Special Weapor.s 
Souadronl 




35 


Project 17 1 ILos Alamos Scientific 
Laboratoryl 


2 


3.5. 3.9 


Radiological Safety 




34 


216lh Chemical Service Company 


'2 


3 3. 3.3 3 4. 34 3 5. 3 6. 40 

4 4449. 61. 9.0 


4925th Test Group" 




4 0.41.42,42.43,48.69 
76 


TOTAL 


50 





' Individual exposures are listed bv name and protect m the film badge records Where ! 

organizations fielded a proieci. specific organization o' participation for an individual c« 

determined 
• Subiect 10 3.9 roentgen AFSWC limii 



•17S 



201 



(^rosby. 




Jeron>c U. Poland, M.D., LTD. 

(218) 546-5108 



One Third Avenue N.E. Crosby, Minnesota 56441 



February 11, 1993 



RE: Albert Parrish 
D.O.B. 10-17-27 



To Whom It may concern: 

Albert Parrish had posterior subcapsular cataract in both eyes. I 
did cataract extractions on May 20, 1988 for the left eye, and 
August 5, 1988 for the right eye. 




Poland M.D. 



202 



Heg:o.-..l Offico B.. '-.■ Hen-y Wh.ppl, 

and Ini.jrBnc. Csnt.i Fee. '.il Bu.lc1.ng 

Fort jnellinq 
St. Paiil MN '. bin 



^, -Votaran? ,; 

,^ : Admin? stratjori :x 



I ' 



JUN 5 1989 ,. ■, . inn.pi»K.t«To. .- 

klbertG. P.crish ^ " "^ °" ^ 



P. 0. Box 236 
Hackensack. MN 56452 



335/211B1 



You also claimed service connection for miscarriages that your wife 
suffered. Ve cannot consider miscarriage as a disability for you. 



C. A. FOYE 
Adjudication Officer 



Enclosure: 

VA Form l-'ilO? 



MG:bje:046SK 




"America is Kl— Thanks lo our Veterans' 



203 



■:poriT OF coriT/ 

NOTE ,J,i, /of„< .......' /.c f.llori ,.u: 



C-er.ter 

St., Paul Jl, Mi-.... 



i 
I 



C ;7 331 Oti3 



Mrs. Albert Parrlsh 



5625 40th .'i venue South, Minneapolis, Minn. 



[J «.»..c Bxt, 



' mFOKMATION IICQULSTtO AMI 



Mrs. Parrish called and stated that a short while ago her husband had 
called at the VA wanting to have a check-up for a disability, and instead 
he had been prevailed upon to file a claim for benefits. He does not 
and is not interested in filing a claim for disability pension but 
merely wanted a hospital check-up if he could have that. 

Mrs. Parrish mentioned several times in the conversation that they did 
not want to file for benefits other than a check-up, and she was told 
the claim would be cancelled. 




Ad judicatic 

; 119 ii; 



204 



Page A6 - Monday, January 3 1 . 1 994 VALLEY MORN ING STAR. Harlingen, Texas 

Gulf War veterans 
wanted for VA study 



ByJOHNCURRAN 

Associated Press Writer 



: BOSTON — The Veterans Ad- 
Rtinistration is mustering Per- 
sian Gulf War veterans together 
in hopes of tracking illnesses and 
ailments plaguing them. 

On Saturday, 88 men and 
women who served in Saudi Ara- 
bia and Kuwait answered the 
call at the local VA hospital, 
some to get treatment, others to 
register for futu re monitorin g. 
^'TheyVe trying. They don^tX 
want another Agent Orange," 
said Larry Hennessy, diagnosed 
with vocal-cord cancer two years 
after he returned from duty. 
After radiation treatments, th 

i ncer went into remis sion 

Hennessy is convinced his ser- 
vice overseas caused it "I think 
it was related to the oil fires and 
the smoke from all the vehicles 
and the space heaters we had in 



the tents," said Hennessy, 42, of 
Randolph. 

He spent seven months work- 
ing as a supply sergeant for an 
engineering unit that built roads 
and paved air strips. He praised 
the VA for seeking out vetefaiib 
and looking at ailment patterns. 

Most of the veterans who came 
Saturday were combat veterans. 
Few had been treated since re- 

t uming home. ___* 

rThoy were given electrocardioA 
grams, counseling, blood tests] 
and other treatment, and re-/ 
ferred to specialists, as neededJ 
There were Post Traumatic 
Stress Disorder counselors, social 
workers and VA representatives 

help them apply for benefits. / 



"A lot of people, when they got 
home from the war, didn't want 
to deal with their medical prob- 
lems. It's important for them to 
register even if the symptoms are 
subtle," said hospital spokes- 
woman Holly Hickson. 



205 



Testimony of 

Thomas M. Goonan 

Vietnam Veteran 

Associate Director 

Agent Orange Family Assistance Program 

Utah State University 

Logan Utah 

to the 

U.S. Senate Committee on Veterans Affairs 

Hearing on Reproductive Hazards Associated 

With Military Service 



August 5, 1994 

10:30 AM 

216 Hart Senate Office Building 



206 



Good morning Mr. Chaimum and mcmbtn of ttie Committae. 

My nam« la Thomas M. Goontn. I Uvc In North Logan, Utah. I am hare 
today becauM I am a huaband of a courageous woman^ the father of two 
children bom with birth defects, a Vietnam veteran, and the Associate 
Program Director for the Agent Orange Family Assistance Program (AOFAF) 
at Utah State University. This program is funded by a grant from the Agent 
Orange Aasiatance Program (AOCAP). 

I serv«d in the Republic of South Vietnam in 1971-1972 In the region known 
as IV Corp". I was stadoned for the majority of my time at the 3rd Surgical 
Hospital CMASH) in Bihn Thuy and at the Can Tho Air Base. During this 
ttme my duties varied from working in the Emergency room, working on 
various wards, and working as an assistant to a maxillo>facial surgeon. In 
Blhn Thuy there was a Navv river patrol unit, Infantry and engineers. The 
perimeter was regularly defoliated with Agent Orange, as wert portians of the 
Mekong River where we drew our drinking water. (This has since been 
validated by one of the dicnts to whom I have provided services through my 
work at Utah State University. His written statements include evidence of 
spraying as weU as having a child widi an oral dleft and learning dlsabllitieB.) 

During my tour, I was a member of a team of medical personnd who flew 
missions to many MAC V/ special forces compounds throughout military 
Region 4 as well as the P.O.W. camps located on Con Son and An Thoy 
Islands. Iliese missions included areas ^t were defoliated by Agent Orange 
during the 1960's and earty 1970's. I returned to the States in Jtme 1972 and 
wu honoraUy discharged in January 1974. 

Upon my return home, I enrolled in college. In 1978 or 79, a woman I was 
dating experienced a spontaneous miscarriage at eight weeks. I began to 
notice large lesions on my shoulders, back and upper anns. I had minor 
surgery to remove a benign tumor frcon the soft palate area. Since that time, I 
have had two s^aceous cysts removed from behind my ears and a TS-gram 
lipoma removed from my left shoulder. I have another lipoma on my left 
forearm. 

In 1984, 1 moved to Utah. I met my wife Mari]ane Llndley, and we were 
married in 1987. Mari]ane WM married previously and had three sons from 
that marriage. There were no complicadons or birth defects associated with 
any of my stsp<«3ns. In 1988, our first son was bom. During the term of that 
pregnancy, Marljane developed preeclampsia / toxemia in her fourth 
month. Michael was bom six weeks premature, weighing 5 poimds, 5 oxmces. 
In addition, our son was bom with an incomplete deft lip- He has had three 



207 



corrective surgerlei since his Urth and Is scheduled for a fourth surgery on 
August li, 1994 - one week from today. 

In 1989, our second son was bom three and a half weeks premature/ weighing 
7 pounds, 10 ounces. Jordan was bom with a unilateral cleft Up / palate, 
Jordan has had four corrective surgeries so far and Is scheduled for two more 
before he enters first grade. 

When Michael was bom, Marijane and I were devastated. I had waited a long 
time to have children. My iiUtial reaction to his birth defect was ttiat it would 
have been better If he had died at birth, d am not proud to admit this, but it Is 
true.) I soon realized that this small child was my son and I had the 
overwhelming responsibility of his stewardship. Corrective surgery or not. 
Mari)ane was deeply distreased by the fact that she did not bear me a perfect 
child. Of course she felt it was her fault. I suspected that Michael's deft Up 
was related to Agent Orange exposure but I did not speak much about it. 
When Jordan was bom in 1989, 1 was depressed and angry. In my mind there 
was no more reasonable doubt that the blrA defects could be traced back 
through my genetic make up. We were counseled by Dr. John Carev, a 
geneticist from the Unlyersity of Utah, and it was determined that since there 
is no history of defts in either side of our famlUes back two generadons that it 
was entirely possible that a parent sperm ceU oould have been mutated by 
dioxln exposure. 

Marijane and I did not apeak of our feeUnga. We did what parents do. We 
provided for our chUdren, but with Indignation. 

In January 1990, 1 began working for the Agent Orange FamUy Assistance 
Prc^ram. Since then, our program at Utah State has worked with 465 famUies 
and 1,097 d\Udren in six states in the western United States and the Nava)o 
and Hopl Indian reservadons. Our In-house data indiates that 17.8 percent 
of the spouses of Vietnam veterans requesKng services from our program 
have had at least one miscarriage. Many have had more; several have had as 
many as five. The divorce rate Is 38.1 percent. Twenty three of the 465 
veterans are deceased, 4 of the 315 spouses are deceased, and 31 of the 1,097 
children are deceased. The average age of Ae ddldren is 16.9 years. 

In working with veterans' families I have found a large group of children 
bom with musculoskeletal deformities, malformed urinary tracts, chUdren 
bom without anal orifices or vaginal openings. These chUdren are born to a 
large portion of the families and are dustered. Some families have several 
children with birth defects and severe learning dlsabUities. The sodo- 
economic status varies, as does the geographic area they are currently Uvlng 
in. The constant b the time served in Vieteam and the Area of Operation. 



208 



m working with veteran families and children with disabllltiefl, there is a 
great void in the types and qxialitv of services available. I have found tlut 
ttiere is no communicatlan or re/erral network between, for example, ttie 
Department of Veterans Affairs, Health and Human Services, and the private 
sector. This tias created an Inhospitable environment for Viemam veterans 
who were treated with contempt when returning ^m the war. The health 
care delivery system is inadequate to meet the needs of veteran families. 
There b no med^anism in the VA or other health care providers which can 
meet dM needs of the veteran family as a xuvit. Referral networks are largely 
non-existent. The services within agencies are categorized and isolated from 
each other placing the burden of the responsibility for health care of the 
patient. 

Thank you for giving toe this opportunity to share this story and my 
experiences with the Committee. 



209 

PREPARED STATEMENT OF KELLI ALBUCK 

Thank you for the opportunity to testify here today. 

My name is KeUi Albuck and I was diagnosed with Gulf War Syndrome at 
the Great Lakes Naval Hospital last week. I was referred by their doctors to 
proceed to Phase n of the DOD Gulf War Protocol. That day they decided I 
was not eligible for medical attention after all. My husband Troy was an 
Airborne Ranger Infantry Officer in the 82d Airborne Division during Desert 
Shield and Desert Storm. He was deployed for 9 months. Currently, my 
husband is totally disabled by Gulf War Syndrome. 

Soon after the return of the soldiers to Fort Bragg, I experienced that upon 
intercourse there was pain and burning. After talking with odier officers' wives, 
I found they had the same experience. On post, we jokingly referred to it as 
"shooting fire." It sounds ftinny, but, it is extremely painful. My first 
miscarriage was December 1991; I was 3 months pregnant. I remember 
thinking, "this happens some times." Beginning in January 1992, I had to see 
civilian doctors because military OB/GYN staff were swamped with a 2-month 
backlog. I received treatment for severe abdominal pain, infectious vaginal 
discharge, headaches, cramping, hemorrhaging, and fever. I felt as though I was 
full of infection. I was tested for sexually transmitted diseases as the cause of 
the pelvic inflammation. However, I have been tested monthly for STDs with 
negative results despite the pelvic inflammatory disease. So the diagnosis 
became asexual pelvic inflammatory disease, which by most doctors' accounts 
is an oxymoron. I continued to see my doctor every other day because of the 
severe pain and to press him for answers. Antibiotics were ineffective, but the 
ultrasound showed cysts on my ovaries. Finally, the doctor decided 
laparoscopic surgery was indicated. 

I became pregnant again in February 1992, we left the Army and relocated 
to Illinois. In the 3rd month I asked my civilian doctor if he knew of any 
problems connected to the Gulf War. He laughed and said, "Oh, no, Mrs. 
Albuck, if there were really any problems, the DOD or medical journals would 
have released notice by now." The baby miscarried 3 weeks later, so we 
switched doctors. I knew something was seriously wrong because my first child 
bom in 1990 was and is fine. During the next couple of months, I was wracked 
with depression, fatigue, chronic abdominal infections, and severe pain (not to 
mention intimacy problems with my husband due to painful intercourse). My 
husband experiences painful, swollen, burning, fluid-filled lesions after 
exposure to his own semen. Sometimes the lesions are bloody and the size of 
half-dollars. He has also been tested for STDs continually, which has caused 
us to eye each other suspiciously at times, but he is clean as of last week. 

By the grace of God, we were blessed with our third pregnancy which gave 
us Alexander. My complications with this pregnancy began at 5 months. I 
hemorrhaged and was hospitalized for 2 weeks. I recaJl my doctor walking in 
the room, in full surgical gear, to tell me that if the heart rate did not climb, 
she would take the baby. Of course the baby would not have lived. We made 
it through 12 more weeks. Alexander was bom 2 months early, weighing only 
three pounds. He faced the following birth problems: Gestationally 
underdeveloped lungs, strep B infection, spinal meningitis, cranial hemorrhage, 
prolapsed heart valve, calcium deposits in kidneys, severe jaundice, bleeding 
ulcers, cerebral palsy, vision and hearing impairments, apnea, respiratory 
distress syndrome, and bronchial pulmonary dysplasia. His half-million dollar 



210 

lifetime limit of health coverage was exhausted in eighty-eight days. His first 
bill (enclosed) is a keepsake. He appears healthy today, but still has many 
problems. For example, I took him to the local emergency room due to 
extremely swollen groin, with severe pain and fever. The doctor had no 
explanation and sent him home with Tylenol. This problem is recurrent and 
topical steroids are only partially effective. My son has been diagnosed with 
yeast infections. We are tired of having illnesses that do not make any sense. 

My husband and I agreed not to have any more children after the ordeal 
with Alexander. Due to Gulf War Syndrome's effects my husband is disabled 
and unable to work so we were financially unable to have sterilization. I was 
on oral contraceptives, fitted for diaphragm to be used with spermicide, and we 
were instructed to use withdrawal to prevent the pain and burning by the 
semen. I was further advised by my doctor not to have any more children due 
to my health. I am currently being seen weekly by my OB/GYN and 
paranatalogist. We were gifted with another pregnancy despite our precautions. 
I have made it through seven months with only one bout of hemorrhage. I am 
still being treated for chronic pelvic infections. I have spoken to. over a 
hundred other female vets and vet spouses to compare tragedies. Because of the 
similarities, I began to ask for more detailed testing of this baby. We are told 
there a deformities with this child too. Their concerns are that the heart is 
malformed and there are extra digits on the left foot, so he may begin with 
more problems than Alexander. We pray everyday that I make it through with 
this child. 

Given the numbers of afflicted spouses and children, it is an obvious failure 
on the part of Congress, DOD, and VA to exclude us from the solutions. It is 
imperative that you include us in any research to determine cause and course 
of treatment of Gulf War Syndrome. We would like to thank the VFW National 
Headquarters for our accommodations. 



PREPARED STATEMENT OF STEPHEN AND BIANCA MILLER 

My name is Stephen Miller. I deployed to Operation Desert Storm with the 
3rd Armored Division out of West Germany during December 1990. At the end 
of January 1991, I returned to Germany due to a shoulder injury. Shortly after 
my return, we conceived our second child. I am currently an active duty 
sergeant stationed at Fort Sam Houston, TX, where I work as a nurse in the 
critical care section. 

Into my wife's twentieth week of pregnancy, an ultrasound determined that 
the baby had hydrocephalus, and a week later an amniocentesis was done. We 
were told that it would take approximately 30 days for the test to be completed. 
After a week we were called in to do a genetic testing on ourselves, as a 
chromosome disorder had been found in our child, along with hydrocephalus 
and spina bifida. This was extremely devastating since our first child was bom 
in March 1990, and she had no problems. Our genetic testing results were 
normal showing no hereditary defects. Shortly after this my wife received 
weekly ultrasounds as we began to prepare for the effects these anomalies 
would have on our child's life. Various physicians counselled us on the effects 
of these anomalies and potential life changes this would incorporate. 

On March 1, 1992, my wife delivered our son Cedrick Miller full term. It 
was then that the full extent of Cedrick' s problems surfaced. Our child was 



211 

missing an eye completely, missing an ear, one side of his face was 
underdeveloped, the heart was on the right side of his body, his trachea and 
esophagus were connected and his thumbs are offset. These anomalies were 
present along with the hydrocephalus and spina bifida, and chromosomal 
defects. At this point, the genetics physician inquired as to what drugs my wife 
and I were using as these anomalies could only be caused by chemical means, 
hereditary, or genetic defects. We asked what they meant, and we were told 
these were a very unusual combination of deformities. I told the physicians I 
was in Operation Desert Storm, and at this point they were quiet. 

Our son was connected to the various life-supporting equipment, and a team 
of doctors were called in to repair Cedrick's tracheal esophageal fistula, and at 
this point we wanted more MRIs done, because the doctors could not tell us 
if Cedrick's brain was normal. We were concerned at this point on, because 
they had informed us of the amount of surgical procedures needed for Cedrick. 
Twenty days and three surgeries later we were allowed to take Cedrick home, 
and to date Cedrick has had eight surgical procedures along with having to be 
fitted for a new prosthetic eye once a month, he continues to be delayed in 
growth and mental development and has feeding difficulties. These feeding 
difficulties are time consuming in that he can only tolerate soft foods, and 
Cedrick in the past has had frequent vomiting episodes several times daily and 
nightly. Cedrick is on the borderline of failure to thrive because of these 
difficulties. Once a month, Cedrick's eye is removed, and his socket is injected 
with a gel to create a mold in order to make a casting for a new eye. Due to 
Cedrick's ventral peritoneal shunt, he must be closely monitored for any 
changes in mental status or physiological changes such as excessive sleep or 
projectile vomiting which are possible indicators of a shunt failure. This could 
be potentially harmful on Cedrick's mental development. Our doctors have 
recommended Cedrick stay out of day care centers to help avoid illnesses as 
even a minor illness can affect his weight gain dramatically which could lead 
to further hospitalizations. 

Prior to deployment, I received six injections. These injections were not 
documented in my medical records. Upon receipt of the pyridostigmine tablets, 
I inquired as to what I was being given, and I was told these tablets were to 
protect us against chemical agents. I was not told of any potential side effects 
or any health risks that might be associated with this product. While taking 
these tablets, I experienced muscle cramping, fatigue, and severe headaches to 
the point that I could not tolerate taking these tablets. I was also issued insect 
repellant containing pesticides. 

In summary, my wife and I feel that this has had a key effect on our son's 
anomalies. We believe this because prior to my deployment, our first child was 
bom healthy without any complications. My wife received good prenatal care 
in Europe and in the United States prior to Cedrick's delivery. Due to 
Cedrick's problems, my wife and I had ourselves genetically tested, and the 
results were normal. Our supporting documents indicate that our son's 
condition may be related to teratogenic exposure. 

This has been an increasing strain on our family, physically, emotionally, 
and financially. 

Thank you for your concern. 



212 




The University orTeime 
Health Science Center at San 

7703 Floyd Curl Drive 

San Antonio, Texas 78284-7836 



Clinical Cytogenetics Laboratory 
Charleen M. Moore, Ph.D., Director 



Room 417F 
(512) 667-5028 



Report of Genetic Laboratory Studies 



Patient: Miller, Bianca 

Date of Birth: 06/20/69 

Date Sample Received: 1 1/27/91 

Referring Laboratory or Physician: Dr. Morales 

Reason for Request: Fetus with multiple midline defects. 



Date of Preliminary Report: 12/05/91 
Date of Final Report: 12/11/91 
Type of Sample: Amniotic Fluid 



Clinical Cytogenetics Laboratory No.: 91-726 

Results: 

46,XY/47^Y,-(-mar 

Chromosomes of 27 cultured amniocytes were counted which were obtained from 4 separate cultures 
These cells had an XY sex chromosome constitution. In each culture two cell lines were identified. Eighteen 
of the cells had a count of 46 with normal chromosomal number and structure. In 9 of the cells a small 
marker chromosome was observed in addition to the other normal 46. This was the size of the short arm of 
the Y chromosome and in some cells had the appearance of a ring chromosome. There was no evidence ot 
satellites or a nucleolus organizing region. Parental chromosomes are recommended to possible determine 
the origin of this marker. If it Is a de novo event, the chance for congenital malformations is approximately 
15%.* 

*Warburtori,Am J Hum Genet 49:995-1013, 1991. 



Qy^^lft, ^ 



6lijLA^ l^^xx^ru^ 



Charleen M. Moore. Ph.D. 

Director 

CytoQcnctics Uboratoiy 



Celia I. Kaye, M.D.. Ph.D. 

Proteuoc of Pediatrics 

Oivuion of Gcnctia and Birth Defects 



213 




The Uaiveraity or Tessa 

Health Science Center at San Antonio 

7703 Floyd Curl Drive 

San Antonio, Tezaa 78284-7836 



Clinical Cytogeaetics Laboratory 
Charleen M. Moore, Ph.D., Director 



Room 417F 
(512) 567-50 



Report of Genetic Laboratory Studies 



Patient: Miller, Stephen S. 

Date of Birth: 02/26/59 

Date Sample Received : 1 2/05/91 

Referring Laboratory or Physician: Dr. Morales 

Reason for Request: Fetus with possible mosaicism. 

Clinical Cytogenetics Laboratory No.: 91-738 

Results: 



Date of Preliminary Report: 12/11/91 
Date of Final Report: 12/11/91 
Type of Sample: Blood 



46,XY 

Chromosomes of 50 PHA-stimulated lymphocytes were counted. These cells had a modal number of 4 
chromosomes. Ten of these cells were analyzed with G-banding and 2 cells were karyotyped. The s« 
chromosome constitution was that of a normal male. No consistent abnormalities were observed in th 
chromosomal number or banding patterns. 



(JUL 



^^, 



/7U5 



Charleen M. Moore, Ph.D. 

Director 

Cytogenetics Laboratory 



Celia I. Kaye, M.O., Ph.D. 

Profcuof of Pediatrics 

Division of Gcnetio and Birth Defects 



214 




The Uaivenity of Tezai 

Health Science Center at San Antonio 

7703 Floyd Curl Drive 

San Antonio, Tezae 78284-7836 



Clinical Cytogenetics Laboratory 
Charleen M. Moore, Ph-D., Director 



Room 417F 
(612) 567-5028 



Report of Genetic Laboratory Studies 



Patient: Miller, Bianca 

Date of Birth: 06/20/69 

Date Sample Received : 1 2/05/9 1 

Referring l-aboratory or Physician: Dr. Morales 

Reason for Request: Fetus with possible mosaicism. 

Clinical Cytogenetics Laboratory No.: 91-739 

Results: 



Date of Preliminary Report: 12/11/91 
Date of Final Report: 12/11/91 
Type of Sample: Blood 



46.XX 

Chromosomes of 51 PHA-stlmulated lymphocytes were counted. These cells had a modal number of • 
chromosomes. Ten of these cells vt*rt analyzed with G-banding and 2 cells were karyotyped. The s. 
chromosome constitution was that of a normal female. No consistent abnormalities were observed in tf 
chromosomal number or banding patterru. 



Ca-.^.«^ 



6Ujl^ 



Charleen M. Moore, Ph.D. 

Oirectof 

Cytogenetics Ubotatory 



Celia I. Kaye 



,M.D.,Ph.O. 



Diviuon of Genetia and Birth OcfcaS 



215 




The Univer»ity of Texas 

Health Science Center at San Antonio 

7703 Floyd Curl Eh-ive 

San Antonio, Texas 78284-7836 



Clinical Cytogenetics Laboratory 
Charleen M. Moore, Pk.D., Director 



Room417F 
(512) S67-S028 



Report of Genetic Laboratory Studies 



Patient; Miller, Infant Male 

Date of Birth: 3/V92 

Date Sample Received: 3/2/92 

Referring Laboratory or Physician : Dr. Stratton 

Reason for Request: Confirmation of Prenatal (91 -726) Diagnosis - 46XY/47,XY, -t- mar 



Dateofrieliminary Report: 3/17/92 
Date of Final Report: 3/20/92 
Typ« of Sample: Blood 



Clinical Cytogenetics Laboratory No.: 92-1 26 

Results: 46,XY/47,XY, -h mar 

Chromosomes of 50 PHA-stimulated lymphocytes were counted. These cells, had a XY sex chromosom* 
constitution. Two cell lines were Identified. Forty-six of the cells (92%) had a count of 46 with norma 
chromosomal number and structure. In 4 of the cells (8%) a small marker chromosome was observed ir 
addition to the other normal 46. This was the size of the short arm of the Y chromosome, and in some cell 
had the appearance of a ring chromosome. There was no evidence of satellites or a nucleolus organizinc 
region. This confirms the prenatal identification of this marker. 



l\) /Vl.w^--_ 



llojojcn^ 



Charleen M. Moore, Ph.D. 

Director 

Cytoqcnetia Lil>or*tory 



Celial. Kaye. M.D..Ph.D. 

Profeuor of Pediatriu 

Oiviiion of Genetia and Birth OefeaS 



216 



The Cause of Reproductive "^^^ diverse nature of the proven toxicants and the senous outcomes 
and Developmental ^^^^ produce suggest that they and other suspected chemical reproduc- 

r)i«M»a««» ^^* *"** developmental hazards deserve serious regulatory considera- 

^"® tion. Several hundred toxicants have been found to produce adverse 

reproductive effects in one or more experimental animals, but since no 
single animal species is a perfect predictor for effects in man, it has been 



CAO/PeMI>«M IcpcodMltv* 1 



difficult to develop a protocol to identify which toxicants should be con- 
sidered potential human hazards. In general, however, animal studies 
have good predictive value for man. 

Human research linking environmental cause and disease is difficult, 
involving as it does, the complications of exposures to no less than the 
three relevant parties: the mother, the father, and the child. Not surpris- 
ingly, several of the best researched toxic agents are drugs. Two exam- 
ples are thalidomide and diethylstilbestrol (dgs), which caused limb 
deformities and cancer, respectively, in offspring. In cases of prescribed 
drugs, doses are often known precisely and the outcomes are dramatic 
and well defined. A nondrug example with a distinct outcome is dbcp, a 
pesticide that through occupational exposure produced absolute male 
infertility. By contrast, most exposures are not so easily measured as in 
drug research and most outcomes are not so dramatic or easily linked to 
an environmental agent Thus, the well-established reproductive and 
devetopmental hazards may be only the tip of the iceberg. 

The cause of most reproductive and developmental disease — more than 
60 percent of it — is unknown. Only 3 percent can now be directly attrib- 
uted to environmental chemicals. Better known causes are disease (such 
as rubella), radiation, or spontaneous mutatk>ns. However, the National 
Research Council believes that some of the disease with no attributable 
cause will be found to be environmentally induced. Thirty-seven percent 
of the experts we surveyed predicted between 10 and 25 percent will be 
found to have an environmental origin. Another 37 percent predicted 
that more than one-quarter of these diseases will be found to have such 
an origin. Since chemical exposure is probably the most preventable 
cause of reproductive disease, we focused on that in our evaluation. 



The Federal Role 



Some 15 federal agencies have mandates assigning environmental health 
responsibilities; however, four agencies are primarily responsible for 
regiilatlng human exposure to chemicals: the Consumer Product Safety 
Commission (Cpsc), the Environmental Protection Agency (cta), the 
Food and Drug Administration (fda) in the Department of Health and 
Human Services, and the Occupational Safety and Health Administra- 
tion (OSHA) in the Department of Labor. 

The lack of scientific knowledge regarding reproductive and develop- 
mental toxicity presents a challenge to the development of a protective 
federal stance. This field has only a scant 40-year history. Data collec- 
tion and understanding of the basic phenomeiu lag several decades 



GAO/PEMDMSI 



217 



DEFIMTIONS 

We have adopted the EPA definitions, quoted here, for the major subfields of male reproductive toxicity, female 
rqjroductive toxicity and developmental toxicity. 

Developmenul Toxicity. The....adverse effects on the developing organism that may result from exposure during 
prenatal development or posmatally to the time of sexual maturation. Adverse developmental effects may be detected 
at any point in the life span of the organism. The major manifestations of developmental toxicity include: ( 1) Death of 
the developing organism. (2) strucniral abnormality, (3) altered giowih. and (4) functional deficiency. 

Female reproductive toxicity. Adverse effects observed in the female reproductive system that may result from 
exposure to chemical or physical agents. Female reproductive toxicity includes, but is not limited to. adverse effects 
observed in sexual behavior, onset of puberty, feitility. gestation, parturition, lactation, or premature reproductive 
senescence. 

Male repi^ductive toxicity. The occurrence of adverse effects on the male reproductive system that may result from 
exposure to environmental agents. The toxicity may be expressed as alterations to the male reproductive organs and/or 
the related endocrine system. The manifestation of such toxicity may include alteration in sexual behavior, fertility, 
pregnancy outcomes, or modifications in otiier functions that are dependent on die integrity of the male reproductive 
system. 

Fbr definitions of the different phases of the risk assessment process, we depend on the National Academy of Sciences 
1983. Risk Assessment in the Federal Government: Managing the Process. 

Risk Assessment. Risk assessment is the qualitative or quantitative characterization of the potential health effects of 
particular substances on individuals or populations. Risk assessment is further divided into 4 sequential steps: hazard 
identification, dose-response assessment, exposure assessment, and risk characterization and is separated logically fror 
risk management, the deliberative step which decides how tiie regulatory body will deal operationally with the agent 

Hazard Identification's] the process of detennining whether exposure to an agent can cause an increase in the 
incidence of a health condition... 

Occupational Groups concern [focuses upon] the ill health effects of factors to which people are exposed in the 
workplace environment, (from Peter Gann. p.302 in Mausner, J. and S. Kramer. Epidemiology, an Introductory Text) 

General Population concern is based on the ill health effects of factors to which people are exposed in non-workplac 
environments. Activities include eating and drinking, breathing indoor and outdoor air. using soaps and cosmetics, 
pursuing habits, etc. Exposures from uncompensated work settings such as childcare and housework are usually placec 
here. 



218 



17 Disorders of the Eye as a Whole 



SUSAN DAY 



Influence of ch* tye on the dcvelopineni of the orbit, 135 



>3S 



Crrptophlhalmoi syndromes. 135 
Microphthalmos. 13s 

I with cyst. 137 
■37 

Cyclopia and synophthalmos. 138 
139 



Influence of the eye on the development 
of the orbit 

Although the absence of a developing eye in itself 
does not affect the initial developtnent of a bony orbit 
(Mann 1937). the growth of the orbit is highly in- 
fluenced by the presence or absence of an eye. At 
birth, the normal eye occupies a higher percentage of 
the orbital volume: growth of the orbital volume 
increases dramatically during the first year of life 
(Peyton 1940). 

How does absence of an eye. either congenitally or 
surgically ai an early age. mtluence the growth of 
the bony orbit? Although orbital volume cannot be 
assessed with X-rays, the horizontal and venicjl 
measurement of the orbital rim can be taken easily. 
Kennedy (1965) has shown that these parameters are 
reduced by 15% in adults who had anophthalmos or 
had the eye removed within the rtrst year of life. He 
has also shown that in humans, cats, and rabbits this 
retardation of orbital growth is approximately halved 
when an orbital implant i>> used and that the severity 
ot the overall reduction in volume diminishes if the 
insult occurs at a later date. Orbital growth appears 10 
be complete by age 15 years, so that subsequent 
enucleation will not result in any appreciable size 
difference. 



Determination of the intluence of an eye on orbital 
volume cannot be detected radiologically. but mea- 
surements of skulls have shown a 60% reduction in 
volume (Kennedy 1973). 

Orbital growth may be secondarily influenced by 
radiotherapy as well (Guyuron a al. 1983). This con- 
sideration as well as intracranial radiotherapy's effects 
becomes important clinically in the management of 
children with retinoblastoma, rhabodomyosarcoma. 
and other radiosensitive neoplasms involving the orbit 
(Starceski et al. 1987). 

Anophthalmos ^- 

Anophthalmos is the term used when the eye is non- 
existent as a true eye or more commonly a tiny cystic 
remnant of the eye is present when the term cryptoph- 
thalmos is preferred. Variable abnormalities of the 
orbit occur. Orbital growth is retarded to some e.xtent 
(Pfeiffer 1945; Kennedy 1965). Extraocular muscles 
may be absent, and optic foramen size decreased 
(Pico & Townsend 1979). The conjunctival sac may be 
very small in size, and its growth must be stimulated 
with insertion of a prosthesis within the first few years 
of life, these prostheses require periodic enlargement 
to continue growth stimulation. 

Anophthalmos represents either a complete failure 
of budding of the optic vesicle or eariy arrest of its 
development. To differentiate between anophthalmos 
and extreme microphthalmos, the examiner can touch 
the lids to feel for any movements representing rudi- 
mentary extraocular muscle function. CT scans may 
demonstrate buried residual soft tissue mass in cases 
of extreme microphthalmos, but histological section- 
ing alone can clarify the presence of neural ectoderm 
derivatives cells or microphthalmos or their absence 
in true anophthalmos (Pearce ci al. 1974-. Brownstein 
c-» al. 1977; Sassani Yanoff t977: Guyer & Green 
1984: Brunquell ct al. 19X4: Peer & BenEzra 1986). 
Unilateral anophthalmos is often associated with 
anomalies of the other eye (0"Keefe a al. 1987) 

Many underlying causes have been proposed for 



135 



219 



136 CHAPTER 17 



anophthalmos. lu bilaterality implies an early een- 
iraliTf ^ rr^ tnpi^ni c event. Most are sporadic 
(Warburg 1981A) although case reports involving sib- 
lings do exist (Zeiter 1963). Chromosomal abnormali- 
ties (Zimmerman & Font 1966; Warburg 1981 b) 
include many syndromes in which extreme microph- 
thalmos is one of many congenital defects. Pre- 
natal infections . X-rays, chemical agents s uch as 
LSD (Bogdanoff ff fl/. IQ72 ) and other environmental. 
agents may all play a role in the anophthalmos- 
microphihalmos spectrum of disorders j Guver & 
Green 1984). Some families have shown a dominant 
gene for coloboma with variable expression with ex- 
treme microphthalmos or cryptophthalmos at one end 
of the spectrum and coloboma, sometimes quite trivial 
at the other. 

The ophthalmologist's management of true anoph- 
thalmos is the same as that of extreme microph- 
thalmos — to stimulate growth of the adnexal 
structures and orbit (Kennedy 1973; Soil 1982). We 
must additionally play a sensitive role in parental 
support of such a child. When bilateral, blindness 
is inevitable and networking with the appropriate 
agencies will provide great support. A search for 
possible causes in conjunction with primary care phys- 
ician may help ease guilt, and genetic counselling will 
aid the parents in understanding risks of future chil- 
dren being involved. When unilateral, emphasis must 
be placed on the integrity of the fellow eye if this is the 
case, and on the relatively normal life that can be 
expected in a monocular child. Safety glasses must be 
considered at an early age to protect the good eye. 



Cryptophthalmos syndromes 

The cryptophthalmos syndrome describes the concur- 
rence of microphthalmos with a varying degree of skin 
covering the eyeball and lids being variably attached 
to the cornea. 

Francois (1969) described three subgroups: 
t Complete cryptophthalmos. The lids are replaced 
by a layer of skin without lashes or glands, and the 
skin is fused with the microphthalmic eye without a 
conjunctival sac. 

2 Incomplete cryptophthalmos. The lids are rudimen- 
tary and there is a small conjunctival sac. The exposed 
cornea is often opaque. 

3 Abortive form. In this form the upper lid is partly 
(used with the upper cornea and conjunctiva. The 
globe IS small. 

The systemic associations include nose deformities, 
clett lip. and palate, syndactyly and many others 



(Francois 1941; Ide & Wollschlaeger 1969: Brazier et 
al. 1986). Surgical treatment is usually unsatisfactory 
and mainly indicated to protea an eye at risk from 
funher deterioration of corneal clarity. 

Microphthalmos 

The spectrum of anophthalmos merges with microph- 
thalmos. The net volume of a microphthalmic eye is 
reduced. Often, clinical suspicion is created on the 
basis of cornea size. Although microphthalmos is 
usually associated with a small cornea, there may be 
microphthalmos with a normal cornea (Bateman 1984) 
and microcornea without microphthalmos (Judisch et 
al. 1979). Ultrasonographic determination of an axial 
length less than 20 mm substantiates a diagnosis of 
microphthalmos (Fran9ois & Goes 1977). Microph- 
thalmos is a relatively rare condition, with an incidence 
of 0.25% (Heimonen et al. 1977) and its prevalence 
accounting for approximately 10% of blind children in 
one study (Fujiki et al. 1982). 

The defect of vision depends on the severity of the 
microphthalmos and whether it is bilateral. 

Microphthalmos can be further divided into colobo- 
matous (Fig. 17. i) and non-colobomotous categories 
(Bateman 1984) on the basis of associated uveal ab- 
normalities. The association between the processes, 
of eye growth and closure of the fetal fissure are 
interiinked and important since closure of the cleft is 
completed eariy in development (Mann 1964). 

Many causal associations of microphthalmos have 
been suggested, and possible causes must be kept in 
mind while considering the child's overall health. 
Bateman (1984) carefully classifies according to here- 
dity, environmental causes, chromosomal aberrations 
and unknown causes which have additional systemic 
abnormalities. Of panicular interest is the cat's eye 
syndrome characterized by uveal coloboma. renal 
malformations, and imperforate anus as a consequence 
of an abnormal chromosome 21 (Schachenmann et al. 
1965; Schinzel et al. 1981) and the CHARGE syn- 
drome in which ocular coloboma with microphthalmos 
are associated with heart defects, choanal atresia, 
retarded growth, genital anomalies, and ear anomalies 
(Hall 1979: Pagonwa/. 1981). Warburg and Friedrich 
(1987) have reviewed the association of coloboma or 
microphthalmos with mental retardation and found 
that multiple chromosomal aberrations can lead to 
these findings. The Lenz microphthalmos syndrome 
includes developmental delay, bat' ears, ptosis, 
dental, digital, and other skeletal, urogenital and 
clefting anomalies (Trabouisi ct al. 1988). 



220 



tin 



. 'nCUUM MOTOR APRAXIA. COGAN CONGeNITAL TYPE 



head low.rd th* obi«ct o< rcg*"*- B*"- "*"• !° *• •»«'~«*^ <**'•« 
Thow . »nd,%"iv/d.vi,hon durin. th. rouhon. Thu h«d 
?^*. U higWy chiractwudc of *e clin.c.1 or«.nUdon. Al»o 
ih^rictemb? is ih. m..nttin«l devi.don of ** eyes when the 
padcnt is rotiled about < verticsl ixis. 

■^In contrast to the defect in voluntary eye movement, the patient 
makes normal random movements of the eyes when not alerted to 
J^kTa volunury fixation. Also, contrasting with the defect of 
horizonul gaze are the noimal vertical movements for all param- 

* ^e°h«d thrusts are usually noted at J-4 months of aee when 
thrmfantle^ns to hold hts hiad erect. Prior to this, the fadu™ to 
Tutate an object may be misinterpreted as indicating blmdness or 
cerebral palsy. General development is typically normal, but the 
cMd tends to be clumsy in spirts and to be a poor reader in the 
first few years of school. Tlie siens and symptoms progressively 
improve during childhood and are not laiown to cause any 
functional defiat in adult life. ^u i ._,< ,>-.„i,i 

SimiUr head thrusts and defects of the vestibular »"<! optoki- 
netic reflexes are seen with au.la letanslyetatla and possibly with 
other defects of the saccadic system, but unlike ""f":^!?!^ V 
motor apraxia, these involve the vertical as weU as the horuontal 



v^p, OUdren are reported to be clumsy and are poor 

readers in the first few years of school. 

Aasodated Finding*: A similar ocular motor syndrome occurs 
f4quently in GaucLc dl.«.. (t>-pe lU), occasiona ly in paoenu 
iXcongenital defects of the midbrain, and rarely m mfants with 
tumors o1 the pontocerebeUar region (two cases). Two as« have 
been reported with brain tumors in the postenor fossa. Several 
cases have been reported with midline structural defects of the 
brain or with vermal aplasia of the cerebellum. 
Etiology: Autosomal recessive inheritance. Several familial cases 
have been documented, including one famUy of apparent domi- 
nant transmission, and one occurrence m •<*«"'"»' '^...Jf^' 

cases occur sporadicaUy unaccompanied by other abnormalities. 

Paihogen«als: Unknown. 

MIMNo.: '216S0 

Sex Ratio: M2J1 

Occurrence: Some fifty cases documented.. 

Risk o( H«eurr«»c» tor PiUenfi Sib: 
See Part I. Mmltlien Inheritanu. 

Risk o» Recurrence lor Patlenfa Child: 
See Part I, Menilelian Inheriunct. 

Age of DeleeUWIIIy: In infancy. 

Gen* Mapping and Unkage: Unknown. 

None known. Genetic counseling indicated. 
Unknown 



Prognosis: Symptoms progressively improve during the first 
two decades of We and are not known to cause any functional 
deficit in the adult. 

Unknown. 



iDG: 



DC, 



al.: A long 



" apraxia. Neuro-ophthaJmol 1980; 
:ogan DC, el al.; Notes on 



n I Ophthalmol 1982: ' 

David C. Cogan 



5*» oPHTHAUMPLeciA. ppocf^essive external 

)cular retraction syndrom* 

U* EYE. OUANE RETRACTION SYNDROME 
)culai-tcollotle type Ehl*r*-O*nlo» syndrom* 

S*t EHLERS-DANLOS SYNDROME 
>culo-acousUc c*r»bral d«s*n*raUon. congenital progreaslv* 

S*» NORRIE DISEASE 



GCULO-AURICULO-VERTEBRAL ANOMALY 

Includes: 

Fado-auriculo-vertebral spectrum 
First and second branchial arch syndrome 
Coldenhar svndrome 
Goldenhar-Corlin syndrome 
Hemifaaal i 



type of congenital ocular motor apraxia presenting |erky 
head movements. Trans Am Acad Ophthalmol Otolaryngol 1932: 
56:153-862. 

Vassella F et al ■ Cogan'j congenital ocular motor apraxu in two 
successive generations. Dev Med Child N'"™'!''^ ,'''_?*?;;"*,, 

iee OS, et al° Congeniul ocuUr motor apraxia. Brain 1977: 100.3«l- 



lollow-up of congenital ocular motor 



S-term lollow-up ( 
mol 1980; 1:H5-1 

tal ocular motor apraxia: assooaled 
ro-ophlhalmology. St. Louis: C.V 
Mosbv, 1980:171-179. 
'jret CH, et al.: Conienital ocular motor apraxia and brain stem 
tumor. Arch Ophthalmol 1980; 98:328-330. 



Acrolsdal dysostosis, Nagw typ* (2167) 

■uxlal typ* (2126) 
((»72) 
dysplssia (2224) 
Charg* assoetatlon (2124) 




073S-U 131-32: Facial asvmmetry secondary to hemifacial 
10123; Coloboma of upper eyelid, abnormal aun- 



des and unilateral facial hypoplasia. 11145: 

strates nght-sided hypoplasia of the face and right mandible. 



221 



OCULO-AUWICUtO-veRTEBBAI. ANOMALY 



I (2615) 
1(0627) 
I dysMietla. TrMchar^oMn* lyp*. racMitv* 

(2802) 
HURCS aMOclaUen (2406) 
Ora-lKle-dlglui tyndrom* 
VMW •uoclaUon (0987) 

Ma|or OlaqnatUc CrlUrta: Exicmal ear nulfomutioni with asso- 
dal«d middle ear anomalin and conductive hearing losi, 
maoosiomia, mandibular hypoplasia, epibulbar dermoids or lipo- 
dermoids. and/or anomalies of^the cervical spine. X-ray may be 
required lo detect vertebral anomalies and facial asvmmetry. 
Microtia or preauricular Ugs may represent the most mild expres- 
sion ol the defect in some famibes. 

Clinical Findings: Variability of expression is characteristic of 
oculo-auriculo-vertebral dysplasia (OAV). Ten to 33% of patients 
have bilateral facial involvement. The disorder is nearly always 
more severe on one side. The right side is involved more severely 
in over 60% of patients. Marked facul asymmetry is present in 
20% of pabents; some degree of asymmetry is evident in 63%. The 
asymmetry may not be apparent in the infant or young child but 
b usually evident by age tour yean. 

The manllary, temporal, and malar bones on the more severely 
involved side mav be small and flattened. The mandibular ramus 
and condyle may' be hypoplastic or absent. Reduced pneumatiza- 
bon of the mastoid region may be observed. 

At least 35% of patients with agenesis of the mandibular ramus 
have associated maaostomia; i.e., lateral facial cleft, usually of a 
mild degree. The macrostomia is almost always unilateral and on 
the more severely affected side. There may bc'associated agenesis 
of the parotid gland. Intraorally, the palate and tongue muscles 

ary from anolia to a 
mildly dysmorphic ear. Approxiitutely one-third of cases show 
bilateral ear involvement. Preauricular tags of skin and cartilage 
are common and may occur anywhere from the tragus lo the angle 
of the mouth. Preauricular sinuses may be present. Narrow or 
atretic external auditory canals may be observed. Small auricles 
with normal architecture may occasionally be seen. Conductive 
and, less frequently, sensorineural hearing loss occurs in the 
iTUjority of patients because of hypoplasia or agenesis of ossicles, 
aberrant facial nerves, and abnormalities of the eustachian tube. 

Blepharophimosis. or narrowing of the palpebral fissure, occurs 
ir. 10% of patients. Anophthalmia or microphthalmia has been 
described, as have retiiul abnormalities. Epibulbar tumors (der- 
moids, lipodermoids) arc found in 35% of patients; they appear as 
solid, yellow or pirik ovoid masses up to 10mm in dumeter. 
Bilateral lesiotu may occur. Vision may be impaired. 

Cervical vertebral fusions occur in 20-25% of patients, and 
Knpp«l-F«il anomaly has occasionally been observed. Platybasia 
and ocapilalizabon of the atlas is found in about 30% of patients. 
Compllcallona: Infants may be small for gestational age and may 
have feeding diiTiculties because of associated cleft lip and/or deit 
palate or an anatomically narrow pharyngeal airway. Obstructive 
sleep apnea has been described. 

Significant visual impairment may be present because of epibul- 
bar tumors or anophihalmiaymicrophthalmia. Removal of epibul- 
bar tumors can lead to scar formation with resulunt leukoma. 

Velopharyngeal insufficiency has been reported unassocialed 
with deft palate. 



aly. microcephaly, skull defects, or intracranial dermoid 
have been reported. Occipital encephalocele has been noted. 
Mental reurdation occurs in 5-15% of the patients, and those with 
cranial defecu are at higher risk. Unilateral or bilateral cleft lip 
and/or palate occurs in 7-15% of patients. Cleft palate is twice as 
common as cleft lip with or without cleft palate. Pulmonary 
anomalies, ranging in seventy from incomplete lobulation to 
unilateral agenesis, have been reported. A vanely of kidney 
abnormalities have been reported, including absent kidney, dou- 
ble ureter, ectopia, hydronephrosis, and hydroureter. 
Congenital heart disease occurs with increased frequency; re- 



appea 
' of sk 



ported inddence figures range from S to 58%. Although no single 
cardiac lesion is characteristic. Ventricular tactal d«l«ct and Hcan, 

car to be the most common. 

skeleul abnormalities have been reported, 
affecting 30% of patients. Spina bifida, anomalous vertebrae, 
scoliosis, and anomalous ribs are relatively common. Talipes 
cquinovanis has been reported m 20% . Umb anomalies may aftect 
approximately 10% of pancnts. Radial lunb anomalies may include 
aplasia of the radius and/or thumb or a bifid or digitalized thumb. 
Etiology; There arc multiple reports of familial cases, with 
widely varymg expression between affected family members. 
Patterns of inhenuncc arc consistent with autosomal domiiunl. 
autosomal recessive, and multi/actorial inheriuncc. Several aber- 
rant karyotypes have been reported. 

PMhog«nMla: May be related to abnormal neural crest cell 
morphology and subsequent malformation of the derivatives of 
the first aivi second visceral arches. Vascular abnormalibcs during 
embryogenesis have produced branchial arch anomalies in ani- 
mals. Jongbloct (1987) suggested a theory of "ovctripencss ovop- 
athy". 

MIM No.: U140. XfAll. 25770 
POSNo.: 3339 
CDC No.: 756.0£0 
S« Ratio: M3:F2 

OccurrMiea: Crabb (1965) observed 1 J.600 birt.Ss in the Midwest 
of the United Sutcs. Another study recorded 1:26.500 live births 
in a prospective study of United Sutcs newborns. No other 
population differences have been reported. 
Riak ol Recurrence tor Pallont't Sib: Empiric recurrence risk is 



Unknown, 
on clinical features. Man- 



Age ol OctecUbllHy: At birth, 
dibular hypoplasia may be i 



usually becomes apparent by age four years. Audiologic evalua- 
tion at an eariy age can detect hcannc loss. High-resolution 
ultrasound may be used for prcnaul detection o( severe car 



u 



helpful in some instances. 



and Linkage: Unknown. 



ton: Avoidance of expgsurcjojcnown jera 
(tuTDeiect and manage assocUleScondu 



manage 
facial < 



loss eariy in life. Repair facial clefts by age six months when 
possible. Speech therapy is often required. Orthodontic and 
dental care to correct malocdusion and other dental anomalies. 
Plastic surgery may improve the facial appearance. Surgical gas- 
trostomy may be required for treatment of /ceding problem. Other 
manifesubons should be treated appropriately. 
Prognosis: Varies with ebology and associated malformations. 
For those patients with no associated chromosomal anomalies or 
other severe associated malformations, life span is norrtul. Five to 
15% have reduced intelligence. Some patients may develop emo- 
tional problems secondary to their faaal defects. 
Detection ol Carrier: Careful evaluarion of first degree relatives 
will help to identify individuals with mild facial manifestations of 
the condition and other extracranial anomalies. 
Special Considerations: Originally, the term hemifacial microsomie 
was used do denote unilateral microtia, macrostomia. and failure 
of the formation of mandibular ramus and condyle. Coldtnhar 
fyndromt referred lo a variant characterued by vertebral anoma- 
lies, most often hemivertebrae, and epibulbar dermoids. FirsI areli 
syndroms and First and iecotid bnnchul arch s^ttdrome were also 
used, but implied that involvement was limited to facial struc- 
tures. 
As evidence emerged that each of these individual terms 



etiologically heterogeneous 

range of dinical expression. Corlin ct al (1963) evolved the term 

Oculo-dunculo-iKrirtral dyiplasia to descnbe the overall condition 



83-529 95-8 



222 



Paternal exposure to chemicals before conception 

Some cUUrenmayb* at risk I 

The dwftn u ctajdnn of nuunul openR to • motr of liiti ■■iiliiiil ■■li miiunl 



t liunnn dtalio* wMh (h< cflcca of 



• thn IK dcttcud onir linr n lift, nich ibocaoat.' Puhm cmplOT<d i 



I riik.' Oher fbrnal t 



dutfc tnaa, !»«»». l<>««OT •oo wwnf -— »™ -"-——- 
mm. lo* otT-ood bbB "ortMi." An iDoweil n«k o( toprefcnyiief 



dbas CO ha prefOiT Thn. dTn 




223 



Marked ir, Search: »55 
'.N: 0019":'7o<= 

:'I: Evidence for Sehavioral Ter atooenici tv in Humans 
lU: Nelson-Bi' 

50: Journal of Aoplied Toxicology, vol. 11. No. 1. pages o3-37. 73 references 
'Y: 1991 

^8: rt brief reviaw was presented of accumulated evidence that prenatal e:<po-3ur9 
,o a number of chemical agents produced behavioral disorders in human beings, 
'opics included: the incidence of mental retardation, developmental 
lisabil i ties, psychological disorders, learning disabilities, and bi rth 
jef ect£ : behavioral disfunctions; established, probable and susp2c:.ad human 
:)ehavioral taratoaens : testing of new drugs; and exposure of cregnjnt women tc 
.■nvi ronmen tal and industrial chemicals. Although many drugs ano an-, ironmentai 
\nd industrial agents have been shown to produce behavioral tarac-oenici tv m 
lumans. the etiology of the vast majority of human .ieveloomen tai iisorde-s has 
jeen unknown. The author concludes that the existence of childhood disorders 
ind dysfunctions, accompanied by a lack of knowleage concerning the etiology of 
;hese disorders, demonstrates the need for aOoitionai research in the fiela of 
ievelopmental neurotoxicology . 

'lE: JJATDK- ; Reproducti ve-system-cisorders ; Teratocenes is- : 

developmental-disorders; Environmental-pollution; Neonates-; imbryo toxici ty- ; 
'.eproductive-hazards; Nervous-system-disorders; E ram-camage ; Neurotoxicology- 



224 



IIQSHTIC usage is subiect to the terms and conditions of the Subscriotion and 

.icense Agreement and the appLicable Copyright and intellectual property 

srotection as dictated by the appropriate laws of your country and/or by 
Cnternational Convention. 

1 of 7 
Marked in Search: »53 
XH: 002160e>0 

ri: Methods and Concepts in Detecting Abnormal Reproductive Outcomes of 
'aternal Origin 
^U: Wyrobek-AJ 

10: Reproductive Toxicology, vol. 7, Supplement i, pages 3-16. 42 references 
'V : 1995 

^6: Methods and concepts for detecting paternal exposures leading to adverse 
■eproductive outcomes were discussed. The role of the father in adverse 
"eproductive outcomes viewed in a mul tigenerational concept was discussed, 
ividenca that certain abnormal reproductive outcomes are of paternal origin was 
:itad. Paternal exposures to chemical toxicants have been shown to be capable 
jf decreasing the quality and quantity of sperm, thereby decreasing fertility. 
Sperm containing cytogenetic abnormalities have been shown to be capable of 
fertilizing eggs. Exposure of the human testes to clastogens increases the 
■'requency of abnormal germ cells. Epidemiological studies have shown that 
lales employed in certain occupations or who have certain occupational 
jxposures have an increased risk of fathering children with birth defects or 
:hildhood cancers. Assessing the functional state of the male reproductive 
system was discussed. Biomarkers that can detect toxic effects in human sperm, 
lamage in male germ cells, and male mediated heritable mutations were 
described. The use of in-vitro systems for investigating the mechanisms of 
lale reproductive toxicity was considered. Biomarkers that can be used to 
)ridge the gap between in-vitro and laboratory animal studies and humans for 
lale reproductive toxicity risk assessment purposes were discussed. 
)E: REPTEO-; Sexual- reproduction ; Reproductive-effects; In-vivo-s tudies : 
eratooenesis- : Spermatogenesis-; In-vitro-studies; Risk-analysis; Genetics-: 
>renatal- exposure 



225 



(N: NTIS P69311S628 

?N: 00? 10242 

ri: Occupational Exposures and Birth Defects 

^U: Mitchell-AA: Louik-C 

30: Slone Epidemiology Unit. Boston University School of nedicine. Brookline, 

lassachusetts. Grant No. R01-0H-0259S , 48 pages. 1'= references 



5Y : 1902 

^B : The utility of the job exposure matrix (JEM) of NIOSH in occupational 
•-eratooen research was assessed. Information was taken from the Slone 
ipidemiology Unit Birth Defects Study i 8DS ) . The JEM was use-3 to assign 
specific workplace exposures to the mothers and fathers of the 11.000 malformed 
Lnfants in the BDS data file. BOS job title/industry codes were translated 
into codes compatible with the JEM. Computer software was developed to produce 
tabulations which provided frequencies of each listed exposure in each bi rth 
Jefect category as well as comparisons to the remaining categories of defects. 
^ detailed exploration of certain aspects of the data was conducted involving 
the testing of a specific hypothesis. Neither the absolute attribution of 
sxposure nor the assessment of exposure probability by the JEM provided a 
:redible measure of exposure. The authors conclude that the NIOSH JEM cannot 
oa usefully applied to the BOS data base to assess risks of occupational 
5xposures in relation to birth defects . 

)E: NIOSH-Publication: NIOSH-Grant; Grant-Number-R01-OH-0259S : End-Date-02-29- 
L992; Reproductive-system-disorders; Reproductive-hazards; Risk-analysis; 
ipidemiology- ; Occupational-exposure 

S of 7 
Marked in Search: «55 
W: 00207450 

ri: Effect of Environmental Agents on Pregnancy Outcomes: Disturbances of 
'renatal Growth and Development 
^U: Cordero-JF 

30: Medical Clinics of North America, Vol. 74, No. 2, pages 279-290, 56 
■ef erences 
'Y: 1990 

^B : Known and potential human teratogens were reviewed and discussed. The 
principles involved in confirming that an agent is a human teratogen were 
•eviewed. Three basic principles are involved; the agent must be taratooenic 
in susceptible animal species; the exposure must occur during a sensitive 
Jeriod of embryogenesis : and the risk of teratocenesis must be dose dependent. 
The first drug to be recognized as a human teratogen was thalidomide (505511. 
Ither drugs di'scovered to be human teratogens included isotretinoin (302794), 
5tretinate (54350480), coumarin derivatives, aminooterin (54626). methotrexate 
59052), penicillamine (52t>75). tetracyclines, phenytoin (57410). and 
/alproic-acid (99661). Environmental chemicals shown to be teratogens included 
nethy l-mercury . lead (7439921), polychlorinated-bipheny 1 ( 133to3';3 ) . 
:,4 ,5-trichlorophenoxyacetic-acid ( ■=37c5 ) and dioxin (1746016). Certain 
lifestyles which predispose persons to teratogens included aloohcl jnd illicit 
irug use. Physical factors known to cause bi rth def ec ts included hypertnermia . 



'E: MCNrtA9- ; Envi ronmen tal -pollu t ion : Or 
'harmaceu ticals- : Lead-poisoning: Pestic 
'evelopmental -disorders : Heavy-me t i Is 



226 






j#i-— —-•-•.'• . 



By KEAY OAViOSON 



defects ■if'- that one spenn cell is 
adversely.affected," Neisoo said. 

i No oncis sure how many birth 

;,.. defects may be "male-mediated," 

i WASHINGTON — Mothers have mainly because ao one is sure what 
been unfairly blamed for genetically causes the majority of birth defects. 
deformed offspring, said researchers \ "Of the 3 percent to 7 percent of 
at the annual meeting of the Ameri- children born with defects detect 
can AssociaUon for the Advance- able at birth, over 60 percent are of 
{■ent of Science. <^ unknown origin," Friedler said. 

TA growing body of data indicates Ironically, the role of men in trans- 
fhat fath^rt j^hy 'fn "'^^ » mafor mitting birth defects was^ accepted 
share of the "blame." bioiogicaiiv 
«p>jiring V»t women have been un- 
jnstlysmgled out for exclusion from 
certain high-risk jobs, ostensibly to 
i>revent birth -defects, scientists said 
At the meetlngof 3,900 s&iUrs and 
Mieiiticts-fnni-'aiouad SKT^world. 
The meeting ended last week. 
ittSSeacanj, scientists tended to <: 
blame a child's developmental de- 
fection some flaw in the mother. But 
r tfaat^uch deforml- 



3 



;> 



exposure toilcofaol. drugs and tbxias ' 
in the.wockplace, speakerssaid. ■ 
; The male'is finally; getting his ' 
doe," said Gladys Friedler, a profes- 
sor of neuropharmacology at Boston' 
U^versity- School of Medicine. 
jjAgreement came from another 
s|eaker, Leonard Nelson, a profes- 
s^fC of physiology and biophysics at 
Vtt Medical CoUege of Ohio. 
■?yDeveloping evidence indicates 
fkat men employed in manufactur- 
ing or agricultural enterprises that 
otHize ha2ardous materials or who 
0&erwise encounter toxicants may 
Ec; responsible for induction of fetal 



during the 19th century. But at the 
time, it was based on shaky evidence 
— for example, degeneracy" theo- 
ries that claimed male indulgence in 
alcohol ancHnigs-ied-to^enetically 
."degenerateT^ds. . 

. ■ - Sn /'h thart^mt fall rm t; nt favnr vith 

the rise of Darwinian biology that 
4X)ttulated,a3fi&wltharhnmU ^ithes 
were transmitted without interfer- 
ence from the environment, such as 
liquor, said historian of science Joy 
ey-of the UniMcsity-of-Okla - 
noma. 

'But 'in' reeenr-decades, *bt link 
'fetween.hirth defects and- the envi- 
ronment has again come under scru- 
tiny. Onereason is bio-disasters such 
as :the Thalidomide scandal of the 
early 1960s, in which a drug taken by 
pregnant women apparently caused 
them to have severely -deformed 
children. 

Unfortunately, in an effort to pro- 
tect fetal health, society has rushed 
to crack down on women while 
letting men off the hook, said Renee 
M. Landers of Boston CoUege Law 
School 



227 



REPROTEXT(R) System 
N,N-D!ETHYL-META-TOLUAMIDE Page 1 of 5 

1.0 ADMINISTRATIVE INFORMATION 

1.1 SYNONYMS 

m-DELPHENE 

m-DETA 

m-TOLUAMIDE, N,N-DIETHYL- 

m-TOLUIC ACID DIETHYLAMIDE 

Al 3-22542 

AUTAN 

BAKER'S ANTIFOL 

BENZAMIDE, N.N-DIETHYL-3-METHYL- 

CHEMFORM 

DEET 

DELPHENE 

DET 

DETA 

DETAMIDE 

DETA-20 

DIELTAMID 

DIETHYL-m-TOLUAMIDE 

DIETHYLTOLUAMIDE 

ENT 20,218 

ENT 22542 

FLYPEL 

M-DET 

METADELPHENE 

MGK DIETHYLTOLUAMIDE 

NAUGATUCK DET 

N,N-DIETHYL-meta-TGLUAMIDE 

N,N-DIETHYL-m-TOLUAMIDE 

N,N-DIETHYL-3-METHYLBENZAMIDE 

OFF 

REPEL 

REPPER-DET 

REPUDIN-SPECIAL 

3-METHYL-N,N-DIETHYLBENZAMIDE 

1.2 IDENTIFIERS 
CAS 134-62-3 

RTECS NUMBER XS3675000 

1.3 FORMDIA 
C12-H17-N-0 

1.4 GENERAL TOXICITY HAZARD RATING 

2 

1.5 REPRODUCTIVE HAZARD RATING 

B 

2.0 INTRODUCTION 

N,N-D!ETHYL-meta-TOLUAMIDE (DEET) is a nearly odorless liquid 
which is soluble in water, alcohol, and ether (Sax, 1985). The 
commercial grade is 85% meta- isomer, with the remainder being 
the ortho- and para- isomoers (HSDB). DEET is one of the most 

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N,N-DIETHYL-META-TOLUAMIDE Page 2 of 5 

widely used insect repellents and is particularly effective 
against mosquitos. Typically the commercial formulations use 
OEET dissolved in ALCOHOL XREF (HSDB). It is the active 
ingredient in OFF!. 

DEET has been extensively studied for its toxic effects. No 
TLV has been established for DEET (ACGIH, 1993). The 
toxicology of DEET has been reviewed (Robbins & Cherniack, 
1986). 

3.0 EPPECTS OP ACTJTE EXPOStJRB 

In acute exposures DEET is not very toxic to animals, with oral 
and dermal LD50"s being in the range of 2 to 5 g/kg and 
inhalation LC50's typically being approximately 5,000 mg/m(3). 
DEET was a primary irritant when applied to the skin or eyes of 
rabbits and has produced desquamation when repeatedly applied 
to humans (HSDB). Rats exposed to 2,300 to 4,000 mg/m(3) for 4 
hours showed behavioral effects (Sherman, 1979). 

4.0 EPPECTS OP CHRONIC EXPOStJRS 

Several fatal cases of overexposure to DEET have occurred in 
children, and exposures greater than 4 grams per week have been 
stated to produce neurotoxic effects (Robbins & Cherniack, 
1 986). Behavioral effects were seen in a child who had been 
heavily treated with DEET over a period of 2 weeks. These 
effects included disorientation, loss of coordination, slurred 
speech, and sudden movements (Gryboski et al, 1961). 

Chfonic usage of DEET can produce very high exposures. In a, 
" rield study OT STViployees at bvergladeS national f»ark, NIOSH 
found that field personnel may use a cumulative dose of 1 00 g ,• 
per week (McConnel et al, 1985). 

When used regularly, the estimated human exposure is 442 grams 
(nearly a pound!) over 6 months (Robbins & Cherniack, 1986). 
DEET has been extensively studied by the US Army, where it was 
used in_field trials. Significant' depot storage occurs in the ■ - 
skirLfronrchrdni(rdermal exposures (Robbins & Cherniack, 1986). 

DEET was not a sensitizer when applied to the skin of guinea 

pigs (Arnbrose et aL 1 959). Behavioral effects were again 

noted in rats and dogs exposed to 250 to 1,500 mg/m(3) for 13 •» i/ 

weeks, and SPERM HEAD ABNORMALITIES we re seen in both species -yfe 

in the s3me study (Macko & Bergman, ISJ'/'S)."' /^ » "* 

Sperm abnormalities were also reported in another paper, but it 
is not clear if this was an original study or a review 
(Gleiberman et al, 1 976). No effects on sperm motility or 
morphology were seen when DEET was applied to the skin of rats 
at 100 to 1,000 mg/kg for 9 weeks, however (Lebowitz et al, 
1983). 

5.0 CARCINOGENIC EPPECTS 

DEET was not carcinogenic in mice or rabbits in a lifetime skin 

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% 



REPROTEXT(R) System 
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painting study (Stenback, 1977). 

6.0 6BIETIC EFFBCTS 

DEET was not mutagenic in the Saimonella/mlcrosome assay (Ames 
test) (Sauers et al, 1 982) and did not induce dominant lethal 
mutations in male mice given a single dose (Swentzel, 1977). 

7.0 RBPRODUCTIVB EPFBCTS 

No Studies were found which examined reproductive effects of 
DEET in humans. 



DEET caused SPERM ABNORMALITIES by inhalation in rats and dogs 
at 1,500 mg/m(3) for 13 weeks (Macko & Bergman, 1979) but had 
no effects on sperm in rats when applied dermally at 1 00 to 
1,000 mg/kg for 9 weeks (Uebowiu et al, 1983). 

DEET was not teratogenic or embryotoxic in rabbits when given 

at 50 to 1 ,000 mg/kg/day from days 1 to 29 of pregnancy ^ 

(An gerhofer & Weeks, 1 981 ) but was teratogenic and embryotoxic ^ 

in-chick*rt*-tKuhlmann et al, 1981). ^bryotoxic and 

developmental effects have been reported in rats (Gleiberman et 

al, 1976). When given dermally to rats at 100 to 1,000 mg/kg, 

the number of implants was reduced and embryotoxicity was seen ' 

but no teratogenicity (Blomquist et al, 1977). 

In a recent study, DEET was not teratogenic and did not affect 
growth or survival of neonatal rats when injected 
subcutaneously at a dose of 0.3 mL/kg/day on days 6 to 1 5 of 
gestation. In the same study, DEET did not affect male 
fertility or induce dominant lethal mutations in males treated 
with doses up to 1 .8 mL/kg/day (Wright et al, 1 992). 

There is some debate in the literature about whether or not 
there is a placental barrier to DEET. In one study a placental 
barrier was seen in mice which were injected (Blomquist et al, 
1975), but no barrier was found when it was applied dermally ^l,»*-« 
(Blomquist et al, 1 977). In_the latter study DEET accumulated '"'^ 
iri the fetuses over the dosing period. However, there was no 
bioaccumulation when DEET was applied to the skin of pregnant 
rabbits (HSDB). 

A review article on DEET states that one report of 
embryotoxicity was not confirmed in other studies (Robbins & 
Cherniack, 1986). There is some confusion in the literature 
about the reproductive effects of DEET in laboratory animals. 
Conflicting results have been found for induction of sperm 
abnormalities, placental transport and embryotoxicity. It is 
not clear if the positive findings for these effects occurred 
in the absence of other toxic signs. DEET appears not to be 
teratogenic but has not been widely studied for teratogenicity. 



) 



8 . PREDISPOSING' CONDITIONS 
MEDICAL: Persons witt 
may be more sensitive. 

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MEDICAL: Persons with eye, skin, or neurological conditions ^ 



230 



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CHEMICAL: DEET did not affect the total absorption of 2,4-D 
dinnethYlaf"lnfl salt through the skin of human volunteers (Moody 
etal, 1992). , 

- AGEt CHILDREN appear to be more' sensitive to DEET;' virtually 
all fatal overdoses have been in children (Anon, 1989). 

11.0 SDMMAHY AND CONCLOSIONS 

DEET is not very toxic to humans or animals but can produce 
neurological and behavioral effects from chronic heavy 
exposures. It is a niild skin and eye irritant. Because of its 
ability to cause neurologicarproblems, DEET is in Class 2 (can 
cause irreversible effects which are not life-threatening) for 
general toxicity. 

The reproductive effects of DEET in laboratory animals are ] 
conflicting with respect to its reported ability to induce j 

sperm abnormalities and embryotoxicity. Because of the "IT 
conflicting results, DEET is in Class B (mixed results, j 

conflicting data) for reproductive hazard. The human I 

reproductive hazard for DEET is unknown. *»* 



12.0 REFSRENCBS 

12.1 GENERAL REFERENCES 

See XREF: GENERAL REFERENCES 

12.2 SPECIFIC REFERENCES 

1 . Anon. Seizures temporally associated with use of deet 
insect repellent - New York and Connecticut. MMWR 
38:678-680, 1989. 

2. ACGIH: 1 993-1 994 Threshold Limit Values for Chemical 
Substances and Physical Agents and Biological Exposure 
Indices. Am Conference Govt Ind Hyg, Inc, Cincinnati OH, 
1993. 

3. AMBROSE AM ET AL. TOXICOL APPL PHARMACOL 1: 97-115,1959 

4. ANGERHOFER RA, WEEKS MH. ISS USAEHA-75-51 -0034-7, ORDER 
NO. AD-A094 778, 22 PP, 1981 

5. Blomquist L & Thorsell W. Distribution and fate of the 
insect repellent (14)C-N,N-diethyl-m-toluamide in the 
animal body. II. Distribution and excretion after 
cutaneous application. Acta Pharmacol Toxicol 41 :235-243, 
1977. 

6. BLOMQUIST L ET AL. ACTA PHARMACOL TOXICOL 37: 121-133, 
1975 

7. GLEIBERMAN SE ET AL. MED PARAZITOL PARAZIT BOLENZN 45: 
65-69, 1976 

8. GRYBOSKIJ ET AL. NEW ENG J MED 264: 289-291,1961 

9. KUHLMANN RS ET AL. TERATOL 23: 48A, 1981 

10. LEBOWITZ H ET AL. DRUG CHEM TOXICOL 6: 379-396,1983 

1 1 . McConnel RS, Smallwood W & Cherniack M. Health Hazard 
Evaluation No 83-085, Preliminary Report. US Public 
Health Service, Centers for Disease Control, National 
Institute for Occupational Safety and Health, Cincinnati, 

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231 



REPROTEXT(R> System 
N,N-DIETHYL-META-TOLUAMIDE Page 5 of 5 

OH, 1985 (cited in Wright et al, 1992). 

1 2. Moody RP, Wester RC, Melendres JL et al. Dermal 
absorption of the phenoxy herbicide 2,4-D dimethylamine 
in humans: effect of DEET and anatomic site. J Toxicol 
Environ Health 36: 241-250, 1992. 

1 3. MACKdJAT BERGMAN" JD7_US ARMY ENVIRON HYGIENE AGENCY.-y 
ABERDEEN PROVING GROUND; STUDY NOr 75-5l'-0034-8b, 42 PP,- ' 

.19791 

14. ROBBINS PJ, CHERNIACK MG. J TOXICOL ENVIRON HEALTH 18: 
503-525, 1986 

15. SAUERS LJ ET AL. GRAI ISS REPORT 1981. LAIR-1 09, ORDER 
NO. AD-A1 07628, 33 PP, 1982 

16. SHERMAN RA. US ARMY ENVIRON HYGIENE AGENCY, ABERDEEN 
PROVING GROUND, STUDY NO. 75-51-0034-80, 27 PP, 1979 

17. STENBACK F. ACTA PHARMACOL TOXICOL 41 : 417-431,1977 

18. SWENTZEL KC. ISS USAEHA-51 -0034-78, ORDER NO. 
AD-A058414, 1 2 PP, 1977 

1 9. Wright DM, Hardin BD, Goad PW et al. Reproductive and 
developmental toxicity of N,N-diethyl-m-toluamide in 

rats. Fundam AppI Toxicol 1 9:33-42, 1 992. 

13.0 AtTTHOR INFORMATION 

Written By: Betty J Dabney, PhD, 03/1 9/88 

Updated By: Betty J Dabney, PhD, 03/92, 09/92, 03/94 

Reviewed By: Alan H Hall, MD, 08/90 



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232 



TERIS - TERATOGEN INFORMATION SYSTEM 
PYRIDOSTIGMINE Page 1 of 1 

Agent Number: 1397 Bibliographic Search Date: 02/93 

Agent Name: PYRIDOSTIGMINE Revision Date: 02/93 

Summary of Teratogenic Effects: 

Pyridostigmine is atireiiS^sterase inhibito^used to treat 
myasthenia gravis, paralytic ileus, and post-operative urinary 
retention. 

MAGNITUDE OF TERATOGENIC 

RISK TO CHILD BORN AFTER 

EXPOSURE DURING GESTATION: UNDETERMINED 

QUALITY AND QUANTITY OF" DATA 

ON WHICH RISK ESTIMATE IS BASED: NONE TO POOR 

COMMENTS: NONE 

No epidemiological studies of congenital anomalies in infants 

born to women who took pyridostigmine during pregnancy have been 

reported. 

The frequency of malformations was not increased among the 
offspring of rats treated during pregnancy with various doses of 
pyridostigmine in a range similar to that used in humans (Levine 
and Parker, 1991). At the highest dose, which produced maternal 
toxicity, increased rate s of_embrvonic death a n d d el a y e d _fgt al 
skeletal ossification were seen. rr-r-irm- .— i= 

Key References: (Each paper is classified as a review [R], 
human case repoa Id, human epidemiological study [E], human 
clinical series |S), animal study (A), or other (0].) 
1) Levine BS, Parker RM: Reproductive and developmental 
toxicity studies of pyridostigmine bromide in rats. Toxicology 
69:291-300, 1991. [A] 



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REPROTOX(TM> System 
V.ESTINON Page 1 of 2 

Pyridostigmine (Mestinone) is an acetylcholinesterase inhibitor 
availabJe_as^the^bromide for the treatment of myasthenia gravis.. 
Neurotransmitters are beli eved, to be irriportant in development of^— ' 
some_pfgan' systerris and iBBW-isrconcern- that alterations '"'"^ >-^ 
neurotransmitter function may disrupt organization of the' '>^ 
central nervous system— This has been examined in neonatal rats 
where pyridostigmine administration has been shown to be 
associated with alterations in brain neuro- transmitter levels 
(1) and in adult behavior (2). It is not known whether 
pyridostigmine influences development in other models. 

There have been a number of case reports of myasthenic women 
treated with pyridostigmine during pregnancy (3-10). Adverse 
effects on the offspring have.not been attributed to drug 
therapy in these reports. The Collaborative Perinatal Project 
also did not find adverse pregnancy outcome to be associated 
with pyridostigmine therapy (11). Eden and Gall (12) presented 
l^jjregnancies-occurring irLajDyasthenic women and concluded 
that prepregnancy thymectomy was the preferred method of 
management. This conclusion was, however, based on ease of 
control and prevention of disease exacerbation rather than on 
adverse effects of pyridostigmine therapy on pregnancy. 
Myasthenic symptoms may be seen in the offspring of some women 
with myasthenia gravis (7); however, this is due to the 
transplacental passage of- immunoglobin directed against 
acetylcholine receptors in muscle, and not to drug toxicity. 

A study in two women showed pyridostigmine to be present in ^^ 
.breas;Ln3iJk la concentrations similar to those in the mothers' Jr^ 
plasrria (13). No drug was detected in the infants and no 
pyridostigmine toxicity was observed. The American Academy of 
Pediatrics and the WHO Working Group on Drugs and Human 
Lactation classified pyridostigmine as compatible with 
breastfeeding (14,15). 

SELECTED REFERENCES 

1 . Dorner G et al: Further evidence of teratogenic effects 
apparently produced by neurotransmitters during brain 
differentiation. Endokrinologie 70:326-30, 1 977. 

2. Domer G et al: Teratopsychogenetic effects apparently 
produced by nonphysiological neurotransmitter concentrations 
during brain differentiation. Endokrinologie 68:1-5, 1976. 

3. Ip MS et al: Thymectomy in myasthenia gravis during 
pregnancy. Postgrad Med J 62:473-4, 1 986. 

4. Giwa-Osagie OF et al: Obstetric performance of patients 
with myasthenia gravis. Int J Gynaecol Obstet 19:267-70, 1981. 

5. McNall PG, Jafarnia MR: Management of myasthenia gravis in 
the obstetric patient. Am J Obstet Gynecol 92:518-25, 1965. 

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234 



REPROTOX(TM) System 
MESTINON Page 2 of 2 

6 Plauche WC: Myasthenia gravis in pregnancy. Am J Obstet 
Gynecol 88:404-9, 1 964. 

7 Plauche WC: Myasthenia gravis in pregnancy: an update. Am 
J "obstet Gynecol 135:691-7, 1979. 

8 Chambers DC et at: Myasthenia gravis and pregnancy. Obstet 
Gynecol 29:597-603, 1967. 

9. Hay DM: Myasthenia gravis and pregnancy. J Obstet Gynaecol 
Br Commonw 76:323-9, 1969. 

10. Rolbin SH et ai: Anesthetic considerations for myasthenia 
gravis and pregnancy. Anesth Analg 57:441-7, 1978. 

1 1 . Heinonen OP et al: Birth Defects and Drugs in Pregnancy, 
Littleton, Publishing Sciences Group, 1 977, pp 345-56. 

1 2. Eden RD, Gall SA: Myasthenia gravis and pregnancy: a 
reappraisal of thymectomy. Obstet Gynecol 62:328-33, 1983. 

13. Harden LI et al: Pyridostigmine in human breast milk. Br 
J Clin Pharmacol 14:565-7, 1982. 

1 4. Committee on Drugs, American Academy of Pediatrics. The 
transfer of drugs and other chemicals into human breast milk. 
Pediatrics 84:924-36, 1 989. 

1 5. The WHO Working Group, Sennet PN (ed).: Drugs and Human 
Lactation. Elsevier, Amsterdam, New York, Oxford, 1 988. pp. 
402-3. 



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235 



To:dc Substances 
Control Act 



This act is administered by the Office of Toxic Substances at gpa. Repro- 
ductive health is mentioned. The objective of the law is "to regulate 
commerce and protect human health and the environment by requiring 
testing and necessary use restrictions on certain chemical 
substances " 



"The health and environmental effects for which standards for the 
development of test data may be prescribed include carcinogenesis, 
mutagenesis, teratogenesis, behavioral disorders, cumulative or syner- 
gistic effects, and any other effect which may present an unreasonable 
risk of iivjury to health or the environment" 

"There is established a committee to make recommendations to the 
Administrator respecting the chemical substances and mixtures to 
which the Administrator should give priority consideration for the pro- 
mulgation of a rule In establishing such list, the committee shall give 

priority attention to those chemical substances and mixtures which are 
known to cause or contribute to or which are suspected of causing or 
contributing to cancer, gene mutations, or birth defects." 

"Upon the receipt of — 

"(1) any test data required to be submitted under this Act, or 



"(2) any other Information available to the Administrator, which indi- 
cates . . . that ... a chemical substance or mixture presents a significant 
risk of serious or widespread harm to human beings from cancer, gene 
muUtions, or birth defects, the Administrator shall . . . Initiate ^>pn>- 
priate action ... to prevent or reduce to a sufficient extent such r^ or 
publish in the Federal Register a finding that such risk is not 
unreasonable." 



236 

PREPARED STATEMENT OF MAUREEN E. PAUL M.D., M.P.H. 

Thank you for the invitation to provide testimony to the Committee on this 
most important topic. I would like to highlight first those aspects of my 
professional training and experience pertinent to my expertise in the area of 
reproductive health hazards. I am to my knowledge one of the very few, if not 
the only, physician in the United States Board-certified in both Obstetrics & 
Gynecology and Occupational Medicine. I received my M.D. from Tufts 
University School of Medicine in 1979, and completed my residency training 
in Obstetrics & Gynecology at the same institution in 1984. For the next three 
years, I was employed as an Assistant Professor at Tufts Medical School and 
as a staff obstetrician-gynecologist at Tufts-New England Medical Center where 
I was involved primarily in clinical work and teaching in reproductive health. 
My interest in occupational and environmental reproductive hazards grew out 
of my clinical experience with patients who increasingly asked questions about 
the effects of workplace, home and community exposures on their reproductive 
health and pregnancy outcomes. In an effort to learn more about this subject, 
I completed a residency program in Occupational Medicine at the University 
of Massachusetts Medical School in 1987 and received my Masters in Public 
Health, majoring in Epidemiology and Environmental Health, from Boston 
University School of Public Health the following year. I was Board-certified 
in Obstetrics & Gynecology in 1986 and in Occupational Medicine in 1989. 

I am currently a faculty member in the Departments of Obstetrics & 
Gynecology and Family & Community Medicine (Division of Occupational and 
Environmental Medicine) at the University of Massachusetts Medical Center 
and Associate Professor at the University of Massachusetts Medical School. In 
1988, I founded and am the Director of the Occupational and Environmental 
Reproductive Hazards Center at the University of Massachusetts which serves 
as a clinical and consultative resource center for employers, health care 
providers, and the public in the area of reproductive health hazards. I have six 
years of intensive clinical experience evaluating and managing patients with 
work-or environment-related reproductive health concerns. I also am engaged 
in research in the areas of occupational reproductive health policy, 
electromagnetic field exposures, and the effects of ergonomic stressors on 
pregnancy outcome. I have published numerous articles on occupational 
reproductive hazards in the scientific literature, and am editor of the only 
comprehensive clinical text on the subject entitled, "Occupational and 
Environmental Reproductive Hazards: A Guide for Clinicians" published by 
William & Wilkins in 1992. As a recognized expert in my field, I have lectured 
extensively on reproductive hazards to audiences ranging from national medical 
and scientific organizations to worker and citizen advocacy groups. I am a 
Fellow of the American College of Obstetricians and Gynecologists (ACOG) 
and the Conte Institute for Environmental Health, as well as a member of 
several national medical societies. I have also participated in a number of 
scientific committees addressing reproductive hazards, serve on the 
Environmental Medicine Committee of the American College of Occupational 
and Environmental Medicine, and have been a consultant on reproductive 
hazards for numerous organizations including ACOG and the General 
Accounting Office of the U.S. Congress. 

I testify today, not only as a health professional with a certain expertise in 
the area of occupational and environmental reproductive health hazards, but 
also as a clinician who is acutely sensitive to the complex social and emotional 



237 

issues that reproductive problems raise for individuals, for families, and for our 
society. Therefore, I would like to express my utmost respect for the veterans 
and their families who are voicing their concerns today. Issues of sexuality and 
reproduction are among the most personal aspects of our lives, and I recognize 
and applaud the courage it requires to share these problems publically. Some 
of our most important scientific breakthroughs in occupational medicine 
occurred because we took seriously and investigated the complaints of a few 
individuals with health problems about which we knew very little. In fact, in 
the 1970s, the entire notion that the reproductive health of men could be 
affected by toxic exposures came about because a few workers exposed to the 
pesticide dibromochloropropane dared to speak up about their sexual problems 
and infertility. Given the significant frequency of adverse reproductive and 
developmental problems in the United States, the causes of which remain 
largely unknown, I believe it is incumbent upon us as scientists and public 
officials to make every effort to increase our understanding of these conditions 
and their etiologies. 

During my testimony today, I will provide a simple overview of 
reproductive health hazards and then succinctly review current scientific 
knowledge regarding the reproductive and developmental effects of some 
specific agents of particular concern to military personnel, including the Persian 
Gulf War veterans. Through this testimony, I hope to show that the subject of 
reproductive health hazards in general, and the complaints of the veterans in 
particular, deserve serious attention and research. 

Overview of Reproductive Health Hazards 

Reproductive function includes a variety of complex processes ranging from 
production of the germ cells (sperm in men and oocytes in women) to sexual 
function to fertilization (union of the oocyte and sperm) to development of the 
fetus and child. There are many points in these reproductive processes at which 
toxic agents can exert their effects. 

In the first place, sexual function can be impaired through exposure to some 
drugs and chemicals. Impotence, for example, has been reported in male 
workers poisoned by lead or manganese. Exposure to toxic agents can interfere 
with the manufacture and growth of the germ cells (sperm or oocytes). Germ 
cell development in both men and women is under the control of chemicals 
called hormones that are released from the brain and from the reproductive 
organs. Possible effects of exposure include menstrual irregularity or early 
menopause, abnormalities in sperm count or other semen parameters, and 
reduced fertility in males or females. 

In the male, sperm production involves an ongoing, constantly renewing 
process of cell division by which men manufacture millions of sperm daily. 
Because men have the capacity to make new sperm in large quantities, toxic 
damage to sperm is often reversible. However, recovery of sperm abnormalities 
and/or fertility may require a number of months or, in some cases, years. Some 
men who were rendered sterile through exposure to the pesticide DBCP, for 
example, took many months to recovery sperm function, and some are still 
sterile years after removal from exposure. 

In contrast to the male, women receive a fixed supply of germ cells before 
birth. The number of oocytes drops from approximately 7 million before birth 



238 

to nearly zero at the time of menopause. During a woman's reproductive years, 
only about 400 of these oocytes are released from the ovary through ovulation, 
while the rest degenerate in a natural process of atresia. 

Toxic agents can disrupt germ cell development by directly damaging the 
sperm or oocytes or by interfering with hormonal regulation of germ cell 
development. Numerous agents have been found to decrease sperm count or to 
affect tihe movement or shape of sperm. Examples include physical agents such 
as heat and ionizing radiation, pesticides such as DBCP and ethylene 
dibromide, and organic solvents such as the ethylene glycol ethers. Less is 
known about germ cell damage in women. However, there is evidence that 
women who smoke cigarettes undergo earlier menopause than non-smokers, 
and animal studies suggest that the polycyclic aromatic hydrocarbons in 
cigarette smoke may cause such effects by accelerating the natural process of 
oocyte degeneration. Hormone production can be disrupted by high levels of 
physical or psychological stress. In addition, environmental chemicals such as 
some organohalide pesticides and polychlorinated biphenyls (PCBs) possess 
estrogenic properties that could interfere with the hormonal regulation of 
reproductive processes. These "environmental estrogens" are the subject of 
intensive study. Abnormal pregnancy outcomes can result from exposures 
before conceprtion or during gestation. Toxic agents can alter the genetic 
material in sperm or oocytes by causing changes in the DNA (mutations) ot in 
whole chromosomes. Genetic damage that is present in the germ cells at the 
time of fertilization can be transmitted to the conceptus, resulting in death of 
the conceptus, congenital malformations, growth or ftmctional deficits, or 
genetic disease, cancer, or sterility in offspring. This is one mechanism by 
which preconception exposures to males could cause abnormal pregnancy 
outcomes. In the dominant lethal test, for example, mating male animals 
exposed to a mutagenic chemical with unexposed female animals can result in 
early pregnancy loss. Other possible mechanisms by which the male could 
affect pregnancy or childhood development, such as the concentration of toxic 
substances in the ejaculate and epigenetic mechanisms, are anply covered in 
Dr. Ellen Silbergeld's testimony. 

While we have a great deal to learn about male-mediated effects in humans, 
increased rates of miscarriage have been reported in the wives of male workers 
exposed to lead, inorganic mercury, anesthetic gases, organic solvents, and 
other agents. Epidemiologic studies also suggest that certain paternal 
occupations may pose an increased risk for the development of childhood 
cancers. For example, some studies have found elevated rates of nervous 
system cancers in the children of men employed in electrical occupations or in 
the petrochemical industry. 

Exposures to pregnant women can affect fetal or childhood development 
through a number of complex genetic, cellular, and biochemical mechanisms. 
The first trimester is when most of the organs of the embryo develop; during 
this period, the emtwyo is most sensitive to teratogens, i.e., agents that cause 
structural birth defects. However, later pregnancy is characterized by fetal 
growth and the continued development and maturation of some organ systems 
such as the nervous, endocrine, and inmiune systems. Therefore, toxic 
exposures after the first trimester can lead to problems such as growth deficits 
or functional or neurobehavioral abnormalities. Some environmental agents that 
are known or suspected teratogens include ionizing radiation, excessive heat, 
ethanol, organic mercury, polychlorinated biphenyls, toluene, and certain 



239 

viruses. Epidemiologic studies suggest that strenuous work may increase the 
risk of preterm deUvery. Increased rates of miscarriage have been found in 
women workers exposed to a variety of agents such as anesthetic gases, organic 
solvents, ethylene oxide, and anticancer drugs. Low-level lead exposure during 
pregnancy has been associated with neurobehavioral problems in offspring. 
Prenatal exposure to diethylstilbestrol (DES) resulted, not only in teratogenic 
effects and decreased fertility in offspring, but also in vaginal cancer. 

In summary, let me highlight some important points. First, we have ample 
evidence from animal and human studies that occupational and environmental 
agents can cause a number of reproductive problems including sexual problems, 
menstrual disorders, and reduced fertility in adults and a wide range of 
abnormalities in fetal and childhood development. Second, reproductive hazards 
affect both women and men, and a growing body of research indicates that 
exposures to the male can affect pregnancy outcome. Third, we still have a 
great deal to learn about the mechanisms by which toxic agents affect 
reproduction, as well as about the effects of specific agents themselves. In fact, 
if one considers that there are approximately 90,000 chemicals in widespread 
commercial use in Western nations, most of which have not been adequately 
tested for reproductive or developmental toxicity, the challenge before scientists 
is quite daunting. 

Specific Exposures in Military Service 

Service in the military can result in exposure to a number of hazardous 
physical, chemical, and biological agents. For the purpose of this testimony, I 
will briefly review what is known about the reproductive effects of ionizing 
radiation, dioxin, and selected pesticides and heavy metals to which Persian 
Gulf War veterans were exposed. A list of the latter agents was provided to me 
by the office of Senator John D. Rockefeller IV. 

Ionizing radiation. Exposure to ionizing radiation can cause a range of 
adverse reproductive and developmental effects by damaging DNA, inhibiting 
cell division, and/or killing cells. A number of factors, such as the dose of 
radiation and the type of tissue exposed, determine what effects occur. Rapidly 
dividing cells of the embryo and dividing germ cells are particularly sensitive 
to radiation damage. Most human data on radiation-induced reproductive effects 
come from studies of populations exposed to high doses of radiation (Japanese 
atomic bomb survivors and patients treated with high doses of radiation); 
extrapolation of these results to the low-dose exposures more commonly 
encountered in the environment is problematic. Ionizing radiation can inhibit 
sperm production at acute exposures of 10-15 rad, and very high doses can 
cause long-term sterility. In general, female germ cells are more resistant to 
killing by radiation than are sperm, although very high doses can result in 
menstrual disturbances or infertility. Older women are more sensitive to the 
sterilizing effects of radiation than younger women, since they have 
significantly fewer germ cells remaining in the ovary. 

Ionizing radiation causes harmful mutations in the germ cells of all species 
of experimental animals. Genetic studies in human populations are extremely 
difficult to carry out. Six indicators of genetic effects (including abnormal 
pregnancy outcomes, childhood mortality, and childhood cancer) have been 
studied in Japanese atomic bomb survivors. Parental exposure to ionizing 
radiation did not result in a statistically significant increase in any one of these 



240 

effects; however, analysis of all effects combined suggested a positive effect. 
One study suggested tfiat an excess of childhood leukemia in the region of a 
British nuclear plant was related to low-dose occupational radiation exposure 
of the fathers in the pre-conception period, but subsequent studies at other 
plants have not confirmed these findings. Another study at the Hanford nuclear 
weapons site found an association between low-dose parental preconception 
exposure to radiation and neural tube defects in offspring. Thus, although 
genetic effects of human preconception exposure to radiation are expected 
based on animal studies, they have not been demonstrated unequivocally in 
humans. Ionizing radiation exposures during pregnancy can cause death of the 
fetus, growth deficits, or congenital malformations, depending on the stage of 
pregnancy at which exposure occurs. Animal and human studies indicate that 
these effects occur at doses of at least 10 rad. The fetal central nervous system 
is very sensitive to ionizing radiation; while mental retardation is well 
documented at high doses, some studies suggest that neurobehavioral deficits 
can occur at lower doses. In addition, several studies suggest that prenatal 
diagnostic radiation exposures below 5 rad may increase the risk of childhood 
leukemia. Studies of Japanese atomic bomb survivors have not confirmed this 
association, although an increased risk for adult tumors that occurred earlier 
than usual in adult life was observed. 

In suntmiary, high dose radiation exposures in humans can cause menstrual 
disorders and reduced fertility or sterility in adults, and exposure during 
pregnancy can have serious effects on fetal development. Although data are 
conflicting, low-dose exposures may increase the risk of genetic conditions and 
childhood leukemia. 

Dioxin. Dioxins are toxic byproducts found in compounds made from 
chlorinated phenols. There are many forms (isomers) of dioxin that vary greatly 
in toxicity. The most toxic is 2,3,7,8-tetrachlorodibenzo-para-dioxin (TCDD), 
the isomer that contaminates the phenoxyherbicide 2,4,5-T. Agent Orange is a 
combination of the phenoxy herbicides 2,4,5-T and 2,4-D, and contains dioxin 
as a contaminant. Dioxin remains in the body for years and persists in the 
environment. 

TCDD (dioxin) is associated with adverse reproductive effects in a number 
of animal species. At high doses, dioxin is toxic to sperm and oocytes. It is a 
powerful teratogen and produces a wide range of developmental abnormalities 
in several animal species including structural defects, growth deficits, fetal 
death, and decreased survival or functional deficits after birth. Dioxin does not 
appear to be mutagenic. Recently, dioxin exposure in monkeys was associated 
with the development of endometriosis. Dioxin may exert some of its effects 
through alteration of reproductive hormonal regulation and immune 
mechanisms. 

Despite the large amount of animal data demonstrating the reproductive 
toxicity of dioxin, the effects of TCDD on humans is still not well delineated. 
Studies have been conducted on humans exposed to TCDD in industrial, 
envu-onmental, and military settings; for the purpose of this testimony, I will 
concentrate on the latter. These studies have design problems that may account 
in part for inconsistent findings, including difficulties in accurately measuring 
exposure to dioxin. 

The Centers for Disease Control (CDC) has reported results of two large 
studies of Vietnam veterans and concluded that the veterans in general did not 



241 

have an increased risk of fathering babies with birth defects (all types 
combined). However, in one study, the risk of certain defects including spina 
bifida, facial clefts, and a miscellaneous constellation of neoplasms was 
elevated in veterans exposed to Agent Orange. In another CDC study, Vietnam 
veterans reported more birth defects in their children than did non- Vietnam 
veterans when interviewed by telephone, but these findings were not supported 
in a smaller subset by examination of hospital birth records. In this study, the 
Vietnam veterans also reported higher rates of pregnancies ending in 
miscarriage and childhood cancers than the non-Vietnam veterans. A report 
from the ongoing Ranch Hand study showed no significant differences 
compared to control groups in outcomes such as prematurity, miscarriages, 
stillbirths or "severe" birth defects. However, an excess of "minor" defects, as 
well as a significant excess of neonatal deaths and physical handicaps, was 
reported. Other studies have reported increases in abnormal outcomes of 
pregnancies fathered by Vietnam veterans including miscarriage and cardiac 
defects in offspring. There have to my knowledge been no consistent findings 
of semen abnormalities or fertility problems in Vietnam veterans. 

In summary, dioxin is highly toxic to reproduction and development in 
several species of animals. Human findings from studies of Vietnam veterans 
exposed to Agent Orange are less consistent but do suggest possible effects on 
fetal and childhood development. Obtaining accurate exposure measurements 
and large enough sample sizes to detect increases in rare defects remain 
significant obstacles to research in this field. 

Exposures to Pesticides and Heavy Metals in Persian Gulf War Veterans. 
Reported exposures to military personnel engaged in the Persian Gulf War 
include fumes and smoke from military operations, oil well fires, diesel 
exhaust, toxic paints, pesticides, heavy metals, depleted uranium, infectious 
agents, chemoprophylactic agents, and multiple immunizations. For the 
purposes of this testimony, I was asked by Senator Rockefeller's office to 
review briefly the suspected reproductive effects of some of the pesticides and 
heavy metal exposures. 

The 18 pesticides that I reviewed include carbamates, organophosphates, 
pyrethrins, anticoagulants, and miscellaneous chemicals. Human data are 
lacking for most of these pesticides, but animal studies suggest that many are 
potential reproductive or developmental toxicants. For example, testicular 
atrophy and decreased sperm counts have been reported in animals exposed to 
lindane, boric acid, and carbaryl. Boric acid is also teratogenic in animals, as 
is pentachlorophenol at high doses. Although little information is available on 
the anticoagulant insecticide diphacinone, it is similar to warfarin which is a 
well-established human teratogen. Other toxic effects on the embryo have been 
reported for many of these substances, and genetic damage has been 
demonstrated for lindane, methomyl, and dichlorvos. 

Of the 7 heavy metals I was asked to review, lead is perhaps the most 
significant since its toxicity in humans is well known. Prenatal exposures to 
lead have been associated with neurobehavioral deficits in infants, growth 
deficits, fetal death, and prematurity. Lead is toxic to sperm and, as Dr. 
Silbergeld's testimony indicates, preconception exposure of male animals to 
lead can also affect fetal brain development. The other metals have not been 
well studied in humans in regard to reproductive effects, but most have been 
tested in experimental animals. Nickel, cadmium, and chromium are toxic to 



242 

sperm in animal studies, and all three are teratogenic. Cadmium is toxic to the 
placenta and has repeatedly been associated with fetal growth deficits. 

Even this cursory review indicates that the Persian Gulf War veterans may 
have been exposed to a number of potential reproductive hazards. In most 
cases, the data are confined to experimental animal studies, and much more 
research is needed to elucidate the effects of these agents on human 
reproduction. 

Conclusion 

As the testimonies today so well illustrate, exposure to potential 
reproductive health hazards in military service is an issue of vital importance. 
There is a tremendous need for more research aimed at explaining the health 
problems experienced by veterans of the Persian Gulf War, including 
reproductive health effects. At the current time we know little about the extent 
of these problems, their manifestations, or whether or not they are linked to 
specific war-time exposures. While we have much to learn about reproductive 
health hazards, it is clear from even the existing data that many military 
exposures have the potential to cause adverse reproductive and developmental 
effects. I urge the Conmiittee to promote well-designed research studies to 
better identify potential hazards and their mechanisms of action, to investigate 
the breadth of reproductive effects experienced by veterans and their families, 
and to explore possible links between suspect exposures and these reproductive 
problems. Giving appropriate attention to this issue provides the opportunity to 
learn more about how environmental agents affect reproductive health, to 
respond to the needs and concerns of veterans, and hopefully to better inform 
and protect military personnel in the future. 

Thank you for the opportunity to submit this invited testimony, and I am 
happy to answer any questions. 



243 



TXSTIM0H7 OF SLLBM K SILBZK0SLO, PH.D. 

before the Senate Coonnlttee oa Veterans Affairs 

August 5, 1994 

ReprodactlTe Health Hazards of Military SerTlce 



244 



I am pleased to present this testimony at the Committee's 
invitation. This testimony is presented in my private capacity; 
I provide the following infonnation on nty professional 
qualifications and appointments by way of informing the 
committee so that it may judge my expertise. I am a 
toxicologist by training; my PhD in environmental engineering 
sciences was obtained from Johns Hopkins, after which I did 
postdoctoral research in environmental medicine and 
(leurosuiences aL Johns Hopkins for Lhcee years. I was Lhen 
employed for 9 years as a research scientist at the National 
Institutes of Health, where I held appointments as chief of the 
neurotoxicology section at NINDS and as a guest scientist in the 
reproductive toxicology section at NICHHD. From 1982 through 
1990 I was primarily employed as senior toxicologist by the 
Environmental Defense Fund. In 1990 I was appointed professor 
of pathology in the Toxicology Program at the University of 
Maryland, a position l still hold although my major appointment 
is now as professor of epidemiology and prevenLive medicine aL 
the University of Maryland Medical School. I am also an adjunct 
professor of health policy and management and of environmental 
health sciences at the Johns Hopkins School of Hygiene. My 
research interests have focussed for many years on mechanisms of 
neurodevelopmental and reproductive toxicology; I have conducted 
research on such toxic substances as lead, manganese, ethanol, 
and TCDD. I have published over 200 scientific papers, reviews. 



245 



and bouk. chapLers. I am a raeuiber uT several i>cleiiLiric and 
honorary scientific societiec; I have received several awards 
and fellowships, most recently a MacArthur Fellowship in 1993. 
My current research interests are in mechanisms of action of 
TCDD and lead, and in understanding ways in which paternal 
exposure to toxic substances can affect the growth and 
development of children. 

In this testimony, I would like to discuss this latter 
topic, because it is potentially significant for evaluating the 
reproducLive risks of exposures in inlliLary service. This is a 
critical area for research at all levels: clinical, 
epidemiological, toxicological, and mechanistic. Fortunately, 
we are acquiring a new understanding of how the paternal 
contribution to reproduction affects early development and later 
disease risks in children. These advances provide us new tools 
for studying specific toxic substances, such as lead, and for 
refining our epidemiological and clinical research projects. 
1. the father's role in reprodactlon and early development 

UtiLil receiiLly, scienLisLs and nonscieuLisLs held a rather 
limited view of the importance of. the father in reproduction and 
development. Obviously, human reproduction is bisexual so that 
the male germ cell is essential for fertiization (although this 
can be accomplished without the direct participation of the 
father, as in the new reproductive technologies of in vitro 
fertiization) . However, it was generally thought that after 
donating his genetic material at the f)oint of fertilization, the 



246 



laLlier played liLLie or i\o iol« in deLecminiiiy Llie ouLcoaie of 
reproduction, that is, the growth of the embryo, fetus, and, 
postnatal ly, the infant. Under this assumption, it was inferred 
that the male could not contribute much damage to reproductive 
outcomes, other than infertility or certain birth defects 
related to the acquisition of genetic damage in the male germ 
cell, the sperm. 

As a consequence, most epidemiological and clinical studies 
were designed to look for reductions in fertility and birth 
delecLsj as midpoints LttaL niighL be ausoclaLed with Lhe exposure 
of fathers. Moreover, it was assumed that since sperm are 
constantly recruited from primordial cells, there was little or 
no possibility of long term or delayed damage: damaging 
exposures had to occur, under these assumptions, during that 
window of time when spermatogonia mature and progress into the 
epididymis prior to ejaculation; only those mature sperm in the 
ejaculate participate in the "lottery" of fertilizing the 
oocyte. Some persons also suggested that some sort of 
Individualized "naLural selection of Lhe fiLLesL" Look place 
during this process, so that any damaged sperm were less likely 
to reach, penetrate or successfully fertilize the ovulated egg. 
It was recognized that exposures of men during the period at 
which conception occurs could be transmitted to the zygote via 
contamination of the ejaculate: the impairments in reproduction 
associated with exposure to cytostatic anticancer agents such as 
cyclophosphamide were shown by Robaire and colleagues to be 



247 



associaLed with Lhe secreLioti oC Llie druy inLo bejiiirial fluid. 

Thus we assumed until relatively recently that the only 
significant exposures of fathers (significant to the offspring) 
occur during the period at which procreation is attempted or 
occurs. Further, we assumed that the major consequence of 
paternal exposures was a reduction in fertility, or an increased 
risk of infertility, although in some rare cases the possibility 
of male-mediated birth defects was considered. 

we now understand that fathers play a much more complex and 
itifluenLial role in early developmeiiL of Lheir children. 
Fathers provide at conception not only half the genetic material 
of the new organisms but also other factors in sperm and seminal 
fluid that are important regulators of very early cell division 
of the fertiized oocyte, later implantation, and early embryonic 
development. This provides additional opportunities for adverse 
influences via paternal exposures to take place. 

In addition, new understanding of the molecular genetics of 
development has resulted in the development of the concept of 
getiomic imprinLiny, which simply staled means LhaL iL sometimes 
matters from which parent you inherited a specific gene. We 
know that for several diseases this phenomenon is the 
determinant of whether or not the functional deficit or 
dysfunction is actually expressed — for retinoblastoma, 
Huntington's disease, and Wilm's tumor there is evidence for 
imprinting. The fact that imprinting exists means that 
genetically "defective" sperm are not selected against at 



248 



£eiLili;iaLion. 

2. Svldcnce for toxic chcsiic^s aff acting aaile xcpxodoetlon and 
developoent of thelz offspring 

Several recent reviews provide compendia on those chemicals 
for which there is evidence of toxic effects to men and their 
children (see Barlow and Sullivan, Ropzoductiv* Bazazd« in th« 
Workplace; Paul, Reproductive Hazards; Mattison and Olshan, Male 
Mediated Effects of Repzodactlon and Develapiaent ) . Several 
compounds are known Lo reduce male ferLiliLy: pesticides aucti 
as dibromochloropropana (DBCP), the glycol ethers, certain 
drugs, radiation, and some solvents. Some of these agents, lilce 
DBCP and radiation, are directly toxic to the male gonad or to 
spermatocytes; others, like solvents, affect neuroendocrine 
signalling that controls sexual maturation, spermatogenesis, and 
even aspects of sexual behavior. 

Relatively few agents have been studied in terms of their 
possible effects on the growth and development of exposed 
faLhers. Aa shown in Table 1, Laken from MaLLison and Olshan, 
epidemiological studies provide a basis for inferring some 
correlations between paternal exposures and a range of adverse 
outcomes in children. It should also be noted, as has been 
stated by two researchers in the field of lead toxicity, Herbert 
Needleman and David Bellinger, that in many cases we have simply 
failed to determine the exposures of fathers, and carried out 
research that focusses by design solely upon the mother's 



249 



exposutea during preynaiicy. In addiLioti, aL leasL in animals, 
it ic well documented that paternal exposures can increase risks 
of transgenerational cancer, that is, tumors appearing in their 
offspring and the offspring of their offspring (review by 
Anderson, in Mattison and Olshan) . 

Epidemiological ly, the strongest evidence exists to 
associate paternal exposures to lead with reduced fertility, 
increased risks of miscarriage, and neurodevelopmental defects 
in children, we are also beginning to develop good animal 
models of these events so LhaL we can begin Lo understand how 
Lead — and possibly other metals — may affect men and their 
children. Lead may act through multiple mechanisms. Lead does 
appear in seminal fluid, and its concentrations are related to 
blood lead levels, although they are much lower. Lead affects 
aspects of the neuroendocrine-gonadal axis, that is, circulating 
levels of such important hormones as LHRH and FSH; those effects 
in some cases are associated with decreased sperm count, 
motility, and ability of sperm to penetrate oocytes. (A recent 
clinical study conducted in Denmark, found eflecLs of lead 
exposure, at relatively low dose, on sperm motility and 
penetration. ) 

In addition, in animals, we find that paternal lead 
exposure, at doses that do not affect fertility, significantly 
affect the early development of embryos and fetuses fathered by 
lead-exposed rats. These effects arc observed as soon as the 
embryo's unique genome is activated, at or about the two-cell 



250 



sLaye of posLleiLili^aLiod developaietiL. LaLer in eitibiyotiic 
develoment, paternal exposure ic acoociated with changes in 
neural development and protein synthesis in the brain of 
neonatal rats. How could these effects occur, and what 
implications may be drawn for human health? It does not appear 
that these effets are related to direct secretion of lead, at 
ejaculation, to the oocyte. These effets are unlikely to b© 
related to major hormonal changes in the male, since they occur 
at doses well below those that affect parameters of reproductive 
success. Ttiese eCIecLa may be related Lo geiioLoxic acLiona of 
lead on sperm, or to epigenetic events involving some of the 
other materials — proteins, enzymes, receptors — that are 
donated by the male to the oocyte at conception. 

The implications for human health, if these mechanistic 
findings can be extrapolated, are several: first, toxic 
substances can affect male reproduction in ways other than 
reduced fertility; second, these effects may occur at doses 
lower than those that cause infertility or subfertiity; third, 
Lhese exposures taay produce long lasting effecLs iti children 
fathered by exposed males; fourth, these effects may be 
expressed as alterations in important functions, such as the 
nervous system, rather than as structural birth defects. 
4. Exposures In Military Service 

Among the substances thought to be toxic to male 
reproduction and the development of children, the heavy metals, 
several pesticides, certain drugs, and radiation are known to 



251 



have advecse eTCecLa, aL LeasL on reproducLive success and In 
some casec upon the development of children. Although a 
relatively limited amount of information has been provided 
concerning exposures in the military, particularly during the 
Gulf War, it is knovm that exposures to heavy metal such as lead 
and cadmium did occur. Moreover, the use of spent uranium did 
subject some US military personnel to uranium exposures. The 
nature and types of pesticide use in the Gulf War is unknown by 
me. Solvents such as the chlorinated ethanes and ethylenes were 
likely Lu have- been used, because of Uieir widespread use in 
cleaning machinery; these agents can affect spermatogenesis. It 
is also possible that adverse reproductive and developmental 
effects (via fathers' exposures) may be associated with drugs 
used licitly and illicitly by military personnel. 

The possibiity of male-mediated reproductive and 
developmental effects was of considerable concern to veterans of 
the Vietnam War. Some data, from the Atlanta Birth Defects 
studies conducted by CUC and from the ongoing Ranch Hand 
followup of Air Force personnel directly involved wiLh Agent 
Orange handling and use, do suggest an association between 
paternal exposures to Agent Orange and increased risks of 
certain birth defects (spina bifida) and neurodevelopmental 
problems in children. Unfortunately, our data on exposure in 
many of these studies are far from complete, as noted by the 
Stellmans in their critiques of CDC and VA studies on Agent 
Orange . 



252 



9. Sesearch Heeda 

This tectimony should have indicated how relatively little 
is knovm of the toxic properties of many agents to which 
military personnel may have been exposed, particularly any 
properties to affect reproduction and development of children 
born to exposed parents. As inventoried by both the EPA and the 
National Research Council, our state of toxicological data 
remains extremely limited. Thus the first research need is 
simply more and better testing of suspect agents, using existing 
LesL meLhods and aieLhods of risk. assessraenL. We need Lo ensure 
that these test methods include comprehesnive evaluation of male 
endpoints, not limited to fertiity as they often are. It is 
also very important to use experimetnal studies to determine the 
timing — including the reversibility or persistence — of any 
effects on male reproductive function and offspring. 

Also, much more information is needed on characterizing 
exposures of military persons to identified repro/dev toxicants 
and other potentially toxic materials, in some cases, it may be 
useful Lo esLablish Lissue banks Lo evaluaLe expusurea and for 
future use as we gain increased knowledge of biological markers 
(of both exposure and early response). In some cases, it may be 
appropriate to establish surveillance mechanisms whereby 
continuing followup of health status, including reproductive 
experience and the develoraent of children, is followed over the 
near and long term. It should be possible to establish these 
functions within the VA medical system, using outside experts to 



253 



advise in Llie desiqii and execuLion o£ sucli studies. 

But the greatest need is in support of basic research, 
without better understanding of hov toxic substances can affect 
men and their children, we will not be able to identify 
potentially toxic agents prior to human exposure, nor will we be 
able to detect adverse effects in exposed populations, new 
developments in molecular genetics and developmental biology 
have helped us not only understand existing epidemiologic and 
experimental data, but they have also stimulated us to examine 
outcomes under condi Lions where paternal functions and 
contributions to development may be at risk. 

Thank you for accepting this invited testimony. I shall be 
happy to answer any questions, and to supply annotations and 
references for this testimony, as requested. 



83-529 95-9 



254 



STATEMENT 



Of 



LINDA SPOONSTER SCHWARTZ RN, MSN 



Before 



SENATE VETERANS AFFAIRS OVERSIGHT HEARING 



on 



REPRODUCTIVE HAZARDS 



August 5,1994 



255 



2022249575 :« 3/12 



INTRODUCTION 

Good Morning Mr. Chairman my name is Linda Spconster Schwartz. I am 
a Retired Major, United States Air Force Nurse Corps and am 
proacncly a Doctoral Candidate ac Yale University School of 
Medicine Department of Epidemiology and Public Health. I am honored 
to have this opportunity to discuss the problem of exposures of 
members of the Armed Forces to toxins and the effects this may have 
on reproductive outcomes and their children. I would like to focus 
my remarks on the effects these exposures may have on women 
veterans who served during the Vietnam Bra. 

Unfortunately, the actual numb©.-- of women who served in Vietnam 
will probably always be in dispute because their exact numbers were 
never recorded. In 1987, the Envlromr.ental Support Group of the 
Department of Defense reported chat their records indicated that 
only 5,905 women were assigned to Vietnam. This number did not 
Include Air Force Flight Nurses assigned outside of Vietnam or 
women who served less than 90 days in the Theater. Often numbers 
between 7,500 and 10,000 are quoted as being a better estimate. 

Research on women veterans has been sparse and limited to small 
numbers. Despite the fact that in November 198"), the VA memdated 
that all future studies of veterans conducted or contracted by VA 
would include women, that has in fact not been the case. As more 
has been learned about the health problems of men who served in 
Vietnam there is a growing concern that the health problems of 
women veterans may also be related to exposure to toxic substances. 



256 



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PAGE 2 
Congressional Hearings by the House Veterans Affairs Committee in 
1983, brought to Liglit Che concerns of women veterans. The most 
prominent witnesses were women vetereuis of the Vietnam War. They 
recounted how they had sought treatment for war related problems 
and had been denied help by the VA because they were not considered 
■Combat Viiterans". Their stories ware pazzicularly poignant when 
they raised questions about the effects of Agent Orzmge on their 
health and the health of their children. 

RESEARCH STUDIES OF WOMEN VETERANS 

As a result of the hearings, the VA oommisaioned Louis Harris and 
Associates to conduct the first systcnatic survey of the current 
status, needs and experiences of women veterans. This study was 
also the first government study to include women of che Vietnam 
Era. In the study, there were 720 women who served during the 
Vietnam War, however only 28 of the group actually served •'Ji the 
Republic of Vietnam. 

The Harris study did look inco specific health problems of "he 
women. Of particular interest 'One of the most striking problems 
of women veterans is cancer. Nearly one out of ten women veterans 
have had a diagnosed case of cancer. This rate of cancer is much 
higher than among the general adult female population. Cancer of 
the uterus, ovaries and cervix (43%) is the leading form of cancer 
among women veterans" . 



257 



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PAGE 3 
In 1988, LeDonne initiated a further analysis of the Harris data. 
Her stu<3y was a comparison of the morbidity of twenty-eight women 
who served in. Vietnam , with 720 women who served in the military 
but not in Vietnam. She fo\ind that Vietnam veteran women had higher 
incidence of chronic health conditions and disabilities, higher 
rates of cancer and higher percen-c.ges of children bom with birth 
defects and/or died before their first birthday. 

At the seune time, Baker, Menard and Johns at the University of 
Texas conducted two studies on the experiences and reactions of 
nuz'ses assigned to Vietnait. which also touched on physiological 
problems. The results of both studies were consistent and 
indicated among other things, that 3 3% of the sample had permanent 
physical disabilities. Major health problems described by the 
nurses at tho time of the study were: recuxrent headaches, skin 
problems, abdominal pain, nausea, and irregularities in menstruation. 

Sharon Rice-Grant at University of California at Sacramento studied 
446 military and civilian women who had been stationed in Vietnom, 
The main thrust of the study was to explore increased physical 
health problems and reproductiv/e outcomes with "perceived" 
exposure to herbicides, including Agent Orange. Particularly 
interesting was her basic premise that so many herbicides and toxic 
chemicals were present in the atmosphere that no specific agent 
could be identified with particular health issues but, rather, the 
effect was more like a toxic cocktail. 



258 



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PAGE 4 
Rice- Grant found that women who served in Vietnam experienced a 
broad range o£ physical problems including soft tissue cancers, 
chronic pain, muscular and psychiatric, memory and concentration 
problema and high rates of birth defects, raiscarriages and 
stillbirths (18.52%) that were associated with perceived exposure 
to Agent Orange. 

Very little attention was paid to these women until Public Law 99- 
272 passed in 1986 authorized and fxmded an ^rideiaiological study 
of the gender specific health effects experienced by women who 
served in the Armed Forces in the Republic of Vietneun. Contracts 
for the development of a protocol for this study were awarded in 
September 1986. Extensive review by the Office of Tecbnology 
Assessment emd the VA ended in an impasse on the approval of the ° 
Women Vietnam Veterans Health Study. • 

NATIONAL VIETNAM VETERANS RcIADJUSTMENT STUDY 

The National Vietnam Veterans Readjustment Study (NWRS) was the 
first government study to include women in any research of that 
veteran generation. The NWRS was a Congress ionally mardated study 
primarily authorized to ascertain the prevalence, incidence and 
effects of Post Traumatic Stress Disorder (PTSD) in Vietnam 
Veterans. The study aimed " to describe comprehensively the total 
life adjustments of Vietnam theater veterans and to compare their 
adjustment with the adjustment of era veterans anJ non veterans." 



259 



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PAGE 5 
The daCa included in this testimony and a similar presentation made 
to the National Academy of Science of the Institute of Medicine 
during it's investigation of the "Health Effects of Herbicides Used 
Ln. Vietnam" came from a secondary analysis of the data collected 
on women from the National Vietnam Veterans Readjustment Study 
(NWRS) . The area of study was limits- to ths self reported health 
problems and reproductive outcomes of the women in the study. 

Th: data from the NWRS provides the first opportunity to compare 
and contrast the self-reported health problems and reproductive 
outcomets of women veterans who served in Vietnam with two groups, 
women veterans who did not serve in Vietnam and civilian women of 
the same age and occupational groups. Within these conparisons 
there is the potential to identify significant health problems 
which may be linked to veterems exposures ajid experiences 
associated with their military service. 

A samgle of 432 Vietnam Theater Veterans (THR) , 3C4 women who 
served during the Vietnam era but were not stationed in Vietnam 
(ERA) and a household sample of 150 nurses and 50 other civilian 
women (CIV) were selected for the study. All three groups of women 
in the study were chosen to have similar occupational status of 80 
% nurses and the civilian au:id Vietnam veteran women were matched so 
that their ages were in the same range. 



260 



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PAGE 6 
The NWR3 is a rich data sec which presents many unique 
possibilities for better understanding vomen Vietnam veterans. 
Although it was not the primary objective of the NWRS to study 
physical health problems, there acre 19 health indicator emd 47 
specific health problem questions . This data represents the most 
extensive attempt to date to assess the health status of women who 
served in Vietnam. In addition to the fact that this is the first 
time these women have been included in such a study, there is the 
added attraction of maJcing comparisons to military women not 
exposed to combat conditions and civiliem women. 

Health Problems 

Questions on the Health Status of women also included infomation 
on the time of onset for each problem. Tn order to mora acc\irataly 
identify problems that occurred as a result of military service, I 
discounted any health problem that occurred before entry into the 
Armed Forces. In order to provide a similar condition for civilian 
women in the study, any illness that occurred before their 
eighteenth birthday, when they would have been eligible for 
military service, was also dropped. 



261 



PAGE 7 
In addition to the health status varicQjles , the NWRS had several 
questions about reproductive outcomes which included total live 
births, miscarriages, tubal pregnancies, stillboms, induced 
abortions and children who died before their first birthday. From 
these outcomes, another VeuriaJsle which reflected the total percent 
of negative reproductive outcomes was created to test the findings 
of previous studies which asserted that women who served in Vietnam 
had higher rates of negative reproductive outcomes. Because a 
distinction was made in the data between misceurriages and induced 
abortions, ' abortions were not counted in the computation of 
negative outcomes because induced abortions were treated as medical 
interventions rather than a spontajxeous outcome. 

REPRODUCTIVE HEALTH AND OUTCOMES 

Women who had served in Vietnam (THR) had significantly higher 
rates of negative reproductive outcomes from their pregnaincies when 
conpared to other military and civilian women in the study. THR 
women had significantly higher rates of- miscarriages and more 
stillbirths, tubal pregnancies and children who -died before their 
first birthday. THR women also had almost twice the rate of cancer 
than did the civilian women. THR women also reported significantly 
higher rates of gynecological diseases of the oveiries and uterus. 



262 



PAGE 8 
These Vietneun veterauis also reported significantly more problems 
that prevented them from working thain did CIV women. One striking 
finding was rates of Multiple Sclerosis which were significantly 
higher for THR women (1.44/100) thcui those reported by other women 
veterems and civilian women. The significeuice of these findings 
held after adjusting for age, marital status, pre-military family 
status and educational attainment. 

EXP0SX7RE TO HERBICIDES 

An added einalysis that was not part of the original data of the 
NWRS was that of exposure to herbicides including Agent Oramge. 
Because the location and dates of duty assignments could be 
determined for each of the THR vetereins as well as number of tours, 
a match was made of this information with the records of Herbicide 
Spraying Missions by Military Regions of Vietnam from 1965-1971. 
Exposure to herbicides was deemed to be that a woman was stationed 
in the Province when the missions were actually being conducted. 

There are many arguments about the insidious nature of toxins and 
their contamination of the food chain amd water supplies and 
therefore anyone stationed in Vietnam after these Missions begam 
could be considered exposed. While a case could be made for this 
inclusive school of thought, I elected to use a more precise albeit 
imperfect measurement of exposure with the idea in mind that this 
approach offered a more rigorous and logical measurement. 



263 



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PAGE 9 
Just as Rice-Grant suggested, tnerc was not one but three 
herbicides recorded as being used during these spraying-- Agents 
Orange, BluG and White-- which supports the notion that no single 
toxin was responsible for any of the ill effects. 

FINDINGS AFTER EXPOSUHS TO HERBICIDES 

Women veterans who were stationed in the Provinces of Vietnam 
during when spraying operations were conducted had higher rates of 
gynecological diseases including uterine ar.d ovarian tumors, 
hysterectomies and and more problems with menses. They also had 
significantly more negative raprnductive outcomes (47.95%) 
than did other women veterans. In fact 28% of these women reported 
that 100% of their efforts to bear children ended in either a 
miscarriage, stillborn or child that died before their first 
birthday. Especially striking were the multiple pregnancies, as 
many as 8 or 9 that ended in the loss of the child and yet 
vmdaunted these women bravely continued to try to become mothers. 

SUMMARY 

Admittedly the NWRS was not designed to be a physical health or 
reproduccive outcome study and other health factors such as smoking 
history were not available. The findings of this analysis are 
meant to provide a basis for additional studies. It is my hope 
that subsequent studies will provide more additional results which 
can assist in planning for the health care of these women veterans. 



264 



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PAGE 10 
One of the most glowing injustices j.n regard to these women is the 
fact that almost twenty years after their service in Vietnam these 
questions go unanswered. No one can know che hear:ibreak of 
wondering if the price of your service is a lost pregnancy or a 
child that struggles with a congenital disabilities. However 
the question of the effects toxins may have on the physical health 
of women who served in Vietnam has not been addressed. • 

There is a need for the Department of Health and Human Services 
include questions in their research on women about military 
service. This would be a cost effective approach to at least 
atten^jting to assfl«s the pro'^lems a~d it would give the added 
opportunity to compare the health of women veterans to women in the 
general adult population. As we approach health care reform, these 
kinds of evaluations will be important for VA to effectively plan 
for the future care of women veterans. 

As we learn more and more eibouc che effects of toxins on other 
groups, women veterans have expressed their fears that th-sy and 
their . children have been forgotten. They voiced particular 
concern aJaout the increasing numbers of early deaths in their 
population. They have also identified several variations of 
autoimmxine diseases, in— j.tero cancers and degenerative processes 
vrtiich seem more than coincide.ital . There is little consolation to 
these women euid their fami"!.- ^s that the VA and CDC report they 
cannot identify a cohort laru-. enough to study the effects of Agent 
Orange or that researchers cannot agree on a methodology for a 
study of health problems of women Vietnam veterans. Each year more 
of the cohort disappears - we bury them . 



265 

STATEMENT OF KWAI-CHEUNG CHAN, ISSUE AREA DIRECTOR, 

PROGRAM EVALUATION AND METHODOLOGY DIVISION, 

UNITED STATES GENERAL ACCOUNTING OFFICE 

Operation Desert Storm: Potential for Reproductive 
Dysfunction Is Not Being Adequately Monitored, gao/t-pemd-94-31 

Mr. Chairman and Members of the Committee: We are here today to present 
our report on possible reproductive dysfunction among the U.S. armed forces 
who served in the Persian Gulf war. My oral statement is based upon the report 
we are issuing today, Operation Desert Storm: Questions Remain on Possible 
Exposure to Reproductive Toxicants. I ask that it and my prepared statement 
be included in the record of this hearing at the conclusion of my oral remarks. 

Since their return from the war in the Persian Gulf, many veterans have 
complained of a variety of health problems including reports of an increased 
number of birth defects and other reproductive problems. It is now known that 
before, during, and after the war, U.S. troops were exposed to a very wide 
variety of potentially hazardous substances. These include but are not limited 
to the following: diesel fuel used as a dust suppressant at encampments, smoke 
from the burning of human and other waste with fuel oil, shower water 
contaminated with fuel, investigational drugs and vaccines to protect against 
chemical and biological weapons, pesticides and insect repellents, and the 
smoke from the oil-well fires at the end of the war. 

My testimony today, and our report, is focused on the potential for 
reproductive effects from these and other substances. The work we did was in 
response to questions the Chairman posed to us this past January. I suimnarize 
those questions and our responses as follows. 

Assessments of Reproductive Toxicants Before the War 

First, What assessments were performed before the gulf war to determine the 
potential for exposure to reproductive toxicants? We found that the assessment 
process that the Department of Defense (DOD) uses for reproductive toxicants 
was incomplete. During DOD's material acquisition process for equipment, it 
performs general health hazard assessments that may identify reproductive 
toxicants, and it relied on the Environmental Protection Agency's normal 
processes for screening pesticides used in the gulf war. However, not included 
in DOD's assessments were potential reproductive effects from various 
individual compounds present in the working environment of deployed troops 
and from the possible synergistic effects of exposure to combinations of 
hazards. These potential effects are currently unknown. 

Reproductive Toxicants Present During the War 

Second, What reproductive toxicants, if any, did DOD actually identify? We 
found that the DOD's health hazard assessment process generally endeavors to 
identify potential reproductive toxicants that are internal to the weapon system 
development process. However, in addition, we found several reproductive 
toxicants that were external to that process and that were not identified by 
DOD. These included reproductive toxicants from the oil-well fires. 



266 

We found a total of 21 reproductive toxicants (listed in appendix I at the end 
of my statement). All these substances were, of course, known to be present in 
the gulf region, and prior scientific research had identified them as potential 
reproductive toxicants. However, up to this point, it has not been pointed out 
that these specific substances present in the gulf region are known reproductive 
toxicants and that an unknown but potentially large number of U.S. troops were 
exposed to them. 

However, we did not ascertain cause-and-effect relationships between 
exposure to these 21 toxicants and reproductive dysfunction reported by 
veterans of the war. Also, the concentration levels of these compounds are 
unknown and so are the exposure rates for specific units. 

Education and Protection Afforded Troops During the War 

Third, What protection and education were provided to military personnel 
to avoid reproductive toxicants during the war? We found none directed 
specifically at reproductive toxicants. However, some activities covered by 
DOD directives to protect against other hazards may have also minimized 
exposure to the reproductive toxicants present. Yet, as we reported earlier, 
some of the protective facilities, equipment, and training were not adequate.' 

DOD did provide some guidance to troops on the toxic hazards of the oil- 
well fires. However, because these fu-es were unanticipated and widespread, it 
was not possible to adequately protect service members from them. This is 
important because we found that several substances in the oil-well fires are 
known reproductive toxicants. 

Monitoring for Reproductive Dysfunction after the War 

Fourth, How are veterans now being monitored for reproductive 
dysfunction? On this point, we found several major shortcomings involving 
certain ongoing and planned studies as well as the Veterans Affairs (VA) and 
DOD registries. 

To begin with, monitoring has not addressed all forms of reproductive 
dysfunction. For example, the VA registry examinations did question veterans 
about birth defects and whether women were pregnant while in the gulf, but the 
registry did not cover other issues such as infertility, miscarriage, and 
additional possible forms of reproductive dysfunction. 

The VA has recently decided to revise its registry questionnaire to include 
questions on infertility and miscarriage. However, the VA has not decided 
whether the 20,000 veterans who have already responded to the earlier, less 
complete, questionnaire will be queried. If they are not, it is possible that data 



'U.S. General Accounting Office, Operation Desert Storm: Army Not Adequately 
Prepared to Deal With Depleted Uranium Contaniination . GAO/NSIAD-93-90 (Washington, 
D.C.: January 1993), and U.S. General Accounting Office. Chemical Wa rfare: Soldiers 
Inadequately Equipped and Trained to Conduct Chemical Operations , 
GAO/NSIAD-9 1-197 (Washington, D.C.: May 1991). 



267 

will not be collected from the very veterans who are most likely to have had 
adverse reproductive health effects. 

Also, a study conducted jointly by the VA, the Centers for Disease Control 
and Prevention (CDC), and the Mississippi State Department of Health assessed 
a high rate of birth defects reported by reserve units in Mississippi. As 
described to us, this unfinished study concludes to date that there was not an 
abnormally high incidence of birth defects among this group compared to a 
group consisting of the overall population of the Atlanta metropolitan area and 
similar data from California and Iowa. 

One of our concerns regarding this study is the possible lack of 
comparability between a group of military reservists and the population of 
urban areas such as Atlanta. While the CDC data constitute a standard set 
accepted among experts, it is reasonable to question whether the Mississippi 
reservists might have been a healthier set of individuals than the general 
population found in urban areas such as Atlanta. In this case, the Mississippi 
reservists would be expected to have a lower rate of birth defects than the rate 
predicted from the Atlanta comparison base rather than an equivalent rate. A 
second concern is that the small size of the Mississippi group makes it difficult 
to detect differences in rates of birth defects unless they are of fairly large 
magnitude. 

Finally, a study to be conducted by the Navy Medical Research Center in 
San Diego, California, plans to examine differences in birth outcomes between 
a large number of gulf veterans and a large comparison group of military 
personnel who were not deployed to the gulf. However, this study will not 
examine records from reserve components and will not collect data on 
infertility and miscarriage rates. 

In summary, questions remain unanswered concerning the potential 
reproductive and developmental dysfunction that may have occurred as a result 
of the Persian Gulf war. The basis for this uncertainty is threefold: (1) certain 
potential reproductive toxicants were indeed present in the region during the 
deployment of U.S. troops; (2) in the case of some of these toxicants, the 
exposures may have been widespread but were of unknown intensity; and (3) 
the studies that have been performed to date are unfinished, cannot be 
generalized, or are too weak methodologically to demonstrate convincingly that 
there are or are not abnormally high reproductive dysfunction rates among 
Persian Gulf veterans and their families. 

Recommendations 

Based on our work, we have four recommendations. 

First, the Secretary of Veterans Affairs should direct that the VA use its 
revised and expanded questionnaire to reregister the 20,000 veterans who have 
already had a VA registry examination. 

Second, the Secretary of Defense, working in concert with the 
Environmental Protection Agency and the Department of Health and Human 
Services, should ensure that DOD makes additional scientific inquiry into the 
possible synergistic effects of multiple exposures to hazards found in the 
Persian Gulf 



268 

Third, the Secretary of Defense should explore approaches to collecting 
baseline data on birth outcomes, infertility, and miscarriage rates among active 
duty and reserve military personnel so that these data are available for future 
studies. This information should also include baseline data on exposure levels 
to ascertain when exposures of reproductive toxicants rise to dangerous levels 
in future conflicts. 

Fourth, DOD should develop procedures to better ensure that troops are 
informed of possible reproductive toxicants before future deployments and to 
monitor exposure levels to such hazards. 

That concludes my testimony, Mr. Chairman; I will be happy to answer any 
questions you or the members of the Committee may have. 

Appendix I 

This appendix lists potential reproductive and developmental toxicants GAO 
found to be present in the Persian Gulf area of U.S. armed forces deployment 
during Operations Desert Shield and Desert Storm. Paternal reproductive 
dysfunction is indicated by tests to determine links to reductions in male 
reproductive capacity, including tests on semen, the endocrine system, fertility 
rates, weight of accessory sex glands, and testes. Maternal reproductive 
dysfunction is indicated by tests on ovaries, the hypothalamus and pituitary, the 
endocrine system, oviducts, uterus, cervix, vulva and vagina, and fertility rates. 
Events that adversely affect the pre-and postnatal development of a child are 
known as developmental, while embryofetal toxicity includes effects on 
survival and development of the embryo or fetus, as well as minor 
malformations and reversible abnormalities. (These are also noted as 
malformations.) The terms given correspond to the scientific literature on which 
the information is based. 

Pesticides 

• Carbaryl, paternal and maternal, malformations 

• Diazinon, malformations 

• Dichlorvos, paternal and maternal, malformations 

• Ethanol, paternal 

• Lindane, paternal and maternal 

• Warfarin, developmental 
Oil Fires and Soil Samples 

• Arsenic, paternal and maternal, developmental 

• Benzene, paternal and maternal 

• Benzo (a) pyrene, paternal and maternal 

• Cadmium, paternal, developmental 

• Di-n-butyl phthalate, paternal 

• Hexachlorobenzene, developmental 

• Hexachlorocyclopentadiene, embryofetal 

• Hexachloroethane, embryofetal 



269 

• Lead, paternal and maternal, developmental 

• Mercury, paternal and maternal, developmental 

• Nickel, paternal and maternal 

• Pentachlorophenol, embryofetal 

• Toluene, paternal and maternal, developmental 

• Xylene, paternal and maternal 
Decontaminating Agents 

• Ethylene glycol monomethyl ether, paternal and maternal 



PREPARED STATEMENT OF SUSAN H. MATHER, M.D., M.P.H., 
ASSISTANT CHIEF MEDICAL DIRECTOR FOR ENVIRONMENTAL 
MEDICINE AND PUBLIC HEALTH, DEPARTMENT OF VETERANS 
AFFAIRS 

Mr. Chairman and distinguished Committee members, the Department of 
Veterans Affairs appreciates this opportunity to appear before the Committee 
to express its deep concern for the health and welfare of all veterans, especially 
those involved in the Persian Gulf conflict, and to describe certain of our 
efforts to respond to their needs. 

Today's hearing focuses attention on the exposure of military personnel to 
substances which have potential reproductive toxicity such as dioxin, pesticides, 
heavy metals, and radiation. VA has targeted programs for illnesses potentially 
related to mustard gas, ionizing radiation. Agent Orange, and Persian Gulf 
service which address the broad range of health effects potentially due to 
known or unrecognized environmental toxins. You have requested that we 
direct our comments today primarily toward an explanation of our ongoing 
programs and investigations related to the reproductive health of Persian Gulf 
veterans. We will also provide a brief update on VA activities related to Agent 
Orange. 

Agent Orange 

Agent Orange is a herbicide which was used as a defoliant by U.S. military 
forces in Vietnam. Dioxin (TCDD) is formed as an unwanted byproduct during 
the manufacture of certain chemicals such as herbicides, fungicides and the 
bactericide hexachlorophene, and was a contaminant of Agent Orange. Dioxin 
can also be produced by incinerators and fossil fuel plants. 

Dioxin is lipophilic and is persistent in fat tissues. It also persists for long 
periods in the environment, particularly in the soil. Analysis of fatty (adipose) 
tissue from the populations of industrialized countries demonstrate the presence 
of dioxins. Among individuals with known histories of high dioxin exposure, 
the levels of TCDD are much higher. 

Because of the evidence pr^.sented in some animal studies of dioxin, studies 
of the long-term health effects in humans have focused primarily on cancer and 
adverse reproductive outcomes. In animals, TCDD is a potent carcinogen and 
has been shown to cause fetal death, birth defects, or spontaneous abortions 
after maternal exposure. Significant species variation in toxicity exists and the 



270 

applicability of this data to human maternal populations is tenuous. To date, 
however, paternal exposure to TCDD has failed to produce any adverse 
pregnancy outcomes in laboratory animals. 

The possibility of fathering a child with birth defects as a result of Agent 
Orange exposure has been a major concern of the Vietnam veterans. There 
have been numerous reports of children born to Vietnam veterans with 
congenital malformations. Although we recognize that the veterans' concerns 
are genuine, there is little or no scientific evidence to support an association 
between military service in Vietnam and subsequent birth defects. 

An important study conducted in 1984 was the CDC Birth Defects Study of 
Vietnam veterans. In this study, children with birth defects among 428 fathers 
who served in Vietnam were compared to children with birth defects among 
268 fathers who were not Vietnam veterans. No association was identified 
between Vietnam veteran status or self-reported Agent Orange exposure and the 
risk of fathering a child with multiple birth defects. 

VA has contracted with the National Academy of Sciences (NAS), Institute 
of Medicine to provide a review of the available scientific literature on the 
health effects of Agent Orange exposure. The results of the NAS committee's 
initial scientific review were published in July 1993, "Veterans and Agent 
Orange". NAS reported that the combined weight of evidence from industrial 
workers, residents living in contaminated areas, and Vietnam veterans studies 
suggests that there is insufficient evidence of a statistical association between 
a father's occupational exposure to herbicides or dioxin and birth defects 
among offspring. The NAS also concluded that there is insufficient evidence 
of a statistical association between adverse reproductive outcomes such as 
stillbirth, neonatal death and infant death, and paternal dioxin exposure. The 
NAS has undertaken an updated review and evaluation of the available 
scientific evidence regarding associations between diseases and exposure to 
dioxin and other chemical compounds in herbicides used in Vietnam. This 
updated review will focus on new scientific studies and literature published 
since the release of the prior report, including those which address the area of 
reproductive health. 

Much of the published science on human exposures to dioxin concerns 
paternal exposures. Because of the continued scientific uncertainty about the 
effects on humans of maternal exposure to dioxin and other environmental 
hazards in Vietnam, VA has initiated the Women Vietnam Veterans 
Reproductive Health Study (PL 99-272). This study will be an important 
advance in our knowledge and understanding of the reproductive health of 
these women veterans. 

Persian Gulf Veterans 

VA has been especially proactive in addressing the health problems of U.S. 
troops who served in the Persian Gulf Even before the fighting in the Gulf was 
completed, the Office of Environmental Medicine and Public Health began 
developing health programs which focussed on the anticipated needs of this, 
our newest, group of wartime veterans. VA's role in determining the potential 
health consequences of participation in the Persian Gulf War has been 
multifaceted. First, VA developed a registry program modeled on the existing 
Agent Orange and Ionizing Radiation Registries. The Persian Gulf Registry is 



271 

designed to provide veterans who have heahh problems or concerns access to 
the VA health system through a comprehensive physical examination, baselinfe 
laboratory testing, and further diagnostic evaluation of identified medical 
problems when indicated. The data obtained from these examinations are 
entered into a computerized database. Although this represents a self-selected 
population and should not be considered an epidemiologic study, our 
Environmental Epidemiology Service closely monitors information in the 
registry to track discemable patterns of illness and health complaints among 
Persian Gulf veterans. The analysis of this information has revealed a wide 
variety of reported symptoms; neither a clear trend of a single diagnostic entity 
nor evidence of the cause(s) of the unexplained illnesses of Persian Gulf 
veterans have emerged. 

From its inception, the Registry protocol has contained questions relating to 
the prevalence of birth defects among children bom before and after Persian 
Gulf service. An analysis of the self-reported data obtained from the first 
17,248 veterans who participated in the Registry examination indicates no 
excess number of birth defects. Registry participants reported that 13,539 
children were bom and 569 (3.3%) had birth defects. Of those children reported 
to have birth defects, 1.5% occurred in children conceived before Persian Gulf 
Service, as compared to 1 .6% of children conceived after service in Southwest 
Asia. 

The Registry is currently being revised to include an expanded number of 
exposure questions, including questions about chemicals and environmental 
hazards which may have the potential to produce reproductive toxicity. 
Furthermore, the reproductive health questions have been expanded to request 
information concerning prevalence of infertility, miscarriages, still births and 
infant deaths. The updated questions focus specifically on both the reproductive 
health concems of veterans and any secondary reproductive effects on their 
spouses. This improved questionnaire design will provide a more detailed 
picture of the reproductive health of Persian Gulf veterans in the near future. 

Persian Gulf Referral Centers 

In addition to the Registry program, VA has established several specialized 
programs to serve Gulf War veterans. First, three clinical referral centers have 
been established at the VA Medical Centers in Houston, Los Angeles, and 
Washington, DC. These tertiary centers perform specialized evaluations for 
veterans whose conditions have evaded diagnosis at their locafVA facility. As 
of July 15, 1994, there have been 126 admissions to these centers. Diagnoses 
in this highly-selected group of veterans suggest a diverse array of disease 
processes and etiologies. Some of the most frequent and severe complaints 
include chronic fatigue, joint pain, headache, muscle aches, diarrhea, short-term 
memory loss or difficulty with concentration, skin rash, abdominal pain, 
shortness of breath and chronic cough, and irritability. Reproductive health 
concerns have not been among the ten most ft-equent complaints in patients 
evaluated by the Registry or of those veterans admitted to the Referral Centers. 
For the veterans who have reported concems about reproductive function, an 
individualized diagnostic work-up is performed. Work-ups may include 
specialized laboratory and diagnostic testing, and subspeciality consultations 
including evaluations by gynecologists, urologists, and endocrinologists. 



272 

Uniform Case Assessment Protocol 

The Departments of Veterans Affairs and Defense have been working 
cooperatively to develop a uniform case assessment protocol for evaluation of 
Persian Gulf veterans with unexplained illnesses. The first step toward 
diagnosis of the health problems of a Persian Gulf veteran is, and will continue 
to be, the Registry examination. If a diagnosis is not readily apparent after 
routine medical evaluations we have recommended that the Comprehensive 
Clinical Evaluation Protocol (CCEP) be used as a set of clinical practice 
guidelines. The CCEP, or uniform case assessment protocol, grew out of the 
medical experience in diagnostic evaluation of Gulf War veterans at the VA 
Referral Centers. The protocol was then further refined and adapted for use by 
both VA and DoD facilities. The CCEP protocol includes a group of 
supplemental baseline laboratory tests and consultations which should be 
provided to every veteran with an unexplained illness. In addition, it gives 
guidelines for the minimum diagnostic work-up of the most frequent complaints 
experienced by Gulf War veterans. This protocol utilizes validated and readily 
available diagnostic tests to thoroughly evaluate each of the common symptoms 
reported by Gulf War veterans. 

The concept behind the protocol was to identify major diagnostic entities 
which could provide an explanation for the symptoms commonly reported in 
Persian Gulf veterans. It should be emphasized however, that the protocol is 
not designed to be all-encompassing but should be carried out with a high 
degree of clinical judgement. All significant symptoms and abnormalities not 
specifically outlined in the protocol, including those concerning reproductive 
health, should be fully evaluated according to the medical judgement of the 
physician who is directing the work-up. The information gathered by this 
process will be entered into a computerized database and will be analyzed for 
patterns of disease. We believe that, in combination with the Registry 
examination, the uniform information obtained through use of the protocol will 
provide the basis for further hypothesis generation and a better understanding 
of the illnesses experienced by Persian Gulf veterans. 

Studies of Reproductive Outcomes in Persian Gulf Veterans 

There are a number of studies in the planning phases which should increase 
our understanding of this issue. The first of these new studies is the Persian 
Gulf Veterans Survey. The Persian Gulf Registry which has been in operation 
for more than two years was primarily initiated to provide health care to 
Persian Gulf veterans who have health problems or concerns after their Service 
in Southwest Asia. More than 24,000 veterans have received examinations 
under the Registry program. The computerized data fi-om the Registry is 
valuable as a surveillance tool and for hypothesis generation but was not 
conceived, nor should it be viewed as an epidemiologic instrument. The self- 
selected nature of the Registry participants makes it a less reliable source of 
information than a randomized study design. Because of this, VA intends to 
conduct a randomized survey of Gulf War veterans. 

A survey of a representative (random) sample of 10,000 veterans and active 
duty members who served in the Persian Gulf is being planned by VA, working 
with DoD and HHS. This mail survey will be designed to determine the 
prevalence of potential exposures experienced by members during their Gulf 
service, symptomatology experienced after Gulf service, their current health 



273 

status including reproductive health, and the health status of family members. 
This group will be compared to a matched group of veterans and military 
members who served in the same era but who were not deployed to the Gulf 
region. A representative sample of eligible respondents will be invited to have 
a health examination as a component of this survey. This survey, because of 
its randomized, controlled study design will provide a more accurate 
assessment of reproductive health and reproductive outcomes than the revised 
Registry examination can provide. 

Another project akeady underway is a study of the children of Persian Gulf 
veterans from the Mississippi National Guard. In response to reports of 
increased rates of birth defects, "rare illnesses" and excessive health problems 
among the children bom to Mississippi National Guard members after service 
in the Persian Gulf War, the Department of Veterans Affairs in Jackson, 
Mississippi, conducted an investigation in collaboration with the Mississippi 
State Health Department and CDC. The study involves a review of the medical 
records of children bom to veterans of the two National Guard units after 
retum from military service in Southwest Asia. The observed medical problems 
in these children were compared to the expected rates of birth defects and other 
health problems. The expected rates of birth defects were obtained from other 
U.S. birth defect surveillance systems, that is the Metropolitan Atlanta 
Congenital Defects Program, and previous surveys such as the Collaborative 
Perinatal Project. 

A preliminary report of the study results shows that of the 282 veterans who 
had served in the two units in the Persian Gulf, 254 (90%) were located and 
interviewed. Fifty-five children had been conceived and born to 52 veterans 
after Persian Gulf service. Medical records were obtained and reviewed on 54 
of the children. The observed number of both major and minor birth defects in 
the study population did not differ from expected. This was a negative study 
and did not identify any overall excess number of birth defects. However, 
because of the small numbers of children included in the study, the 
investigators were unable to definitively determine whether the observed 
number of specific birth defects identified among this group was greater than 
expected in the general population. 

The numbers of children in the study group who were born prematurely 
and\or with low birth weight was similar to that in the U.S. population. No 
stillbirths or neonatal deaths had occurred. 

This small descriptive study does not identify an increased rate of major or 
minor birth defects or an increased risk of prematurity among the study group. 
A more formal case-control study with a larger number of subjects is required 
to determine possible risk factors for birth defects or other adverse birth 
outcomes among children born to military personnel. 

National Academy of Sciences Study on Persian Gulf 

VA and DOD have jointly entered into a contract with the NAS to study the 
possible health consequences of service in the Persian Gulf. The contract with 
the NAS was awarded in September 1993 and two Committee meetings have 
been held. We are hopeful that the NAS review will provide valuable scientific 
insight into the unexplained illnesses of Persian Gulf veterans. An interim 
report is expected in late 1994. 



274 

Mr. Chairman, with regard to decisions of service connection for disability 
or death associated with veterans reproductive systems, generally the same 
rules of direct and presumptive service connection apply as are used for other 
disabilities. Sections of the VA schedule for rating disabilities, 38 CFR Pt.4, 
specific to the genitourinary and gynecological systems are used to evaluate 
disability due to disease or injury incurred in or caused by military service. 
Additional monthly compensation set by law is payable in the event of the loss 
or the loss of use of a creative organ, 38 USC 1 1 14(K). 

Conclusion 

Historically, the most imminent hazard of warfare is physical injury related 
to armed conflict, although infectious diseases have also been a frequent threat 
to service men and women in war time. In addition, recent experience has 
irrefutably demonstrated that there are also significant toxicologic and 
environmental hazards associated with modem warfare. In all of our clinical 
and research efforts, the VA will continue to pursue explanations for the 
illnesses experienced by U.S. veterans and develop innovative programs to 
return them to good heaJth. VA is fully committed to investigate all plausible 
causes for poor health and adverse reproductive outcomes. We look forward to 
working with the Committee towards this mutual goal. 

Mr. Chairman, I would like to thank you for the opportunity to discuss VA's 
efforts to assist veterans who were exposed to hazardous substances while they 
bravely served their country. 



STATEMENT OF HENRY FALK, M.D., NATIONAL CENTER FOR 

ENVIRONMENTAL HEALTH, CENTERS FOR DISEASE CONTROL 

AND PREVENTION, PUBLIC HEALTH SERVICE 

I am Dr. Henry Falk, Director of the Division of Environmental Hazards and 
Health Effects, National Center for Environmental Health, Centers for Disease 
Control and Prevention (CDC). Accompanying me today, is Dr. Coleen Boyle, 
Chief, Surveillance and Epidemiology Section, Developmental Disabilities 
Branch, Division of Birth Defects and Developmental Disabilities, National 
Center for Environmental Health, CDC. CDC is pleased to have this 
opportunity to suggest ways that we can assist the Departments of Defense and 
Veterans Affairs in determining whether veterans are at high risk for 
reproductive dysfunction such as infertility, cancer of the reproductive system, 
and abnormal birth outcomes. As you know, we have assisted in similar matters 
through previous studies of the health of Vietnam veterans and birth defects in 
their children, and with these as a guide we have some suggestions for ways 
that we could help with the study of these reproductive outcomes in the future. 

In the late 1970s, veterans of the U.S. military effort in Vietnam became 
concerned that exposure to Agent Orange may have increased their risk for 
fathering babies with birth defects. In 1981, CDC investigated this matter using 
a birth defects registry in Metropolitan Atlanta. This registry, supported by 
CDC, permitted us to mount a large epidemiologic case-control study, adding 
information gathered from interviews with male veterans and their wives. The 
results of the study showed that U.S. veterans of the Vietnam conflict were not 
at higher risk of fathering babies with birth defects than were other veterans or 
men in the general United States population. This study also yielded 



275 

information that proved valuable in addressing other questions about the causes 
of birth defects. For example, data from the veterans study showed that women 
who took supplemental vitamins before and during pregnancy had a decreased 
risk of having an infant with a neural tube defect such as spina bifida or 
anencephaly. These data were part of the scientific basis for the Public Health 
Service recommendation for the consumption of the B vitamin folic acid for the 
prevention of spina bifida and anencephaly, a birth defect that is particularly 
high in several geographic areas in the United States. This recommendation 
was published in the CDC Morbidity and Mortality Weekly Report in 1992. 

In addition, CDC, through an interagency agreement with the Department 
of Veterans Affairs, carried out the Congressionally mandated studies of the 
effects of Agent Orange and die Viemam experience on the health of American 
Vietnam veterans. The CDC Vietnam Experience Study was an historical 
cohort study of the morbidity and mortality patterns in a sample of U.S. Army 
Vietnam War-era veterans who did not serve in Vietnam. The cohort of 18,000 
male veterans was randomly chosen from among men who had served in the 
U.S. military during the Vietnam War era. The Vietnam Experience Study 
collected information on veterans health problems, including information on 
reproductive health, such as, infertility problems and reproductive cancer. In 
addition, information was collected on a wide range of health problems in 
children born to Vietnam War veterans, including birth defects and 
developmental problems. This study showed that Vietnam veterans were more 
likely to report difficulties in conceiving pregnancies than were Vietnam-era 
veterans. They were also more likely to have sperm abnormalities, however, 
there were no significant differences in the average number of children 
fathered. In addition, the results of this study showed that Vietnam veterans 
were at increased risk for several nonreproductive conditions, such as post- 
traumatic stress disorder. 

At the suggestion of the House Committee on Veterans' Affairs Chairman, 
Sonny Montgomery, the State of Mississippi and the VA, CDC recently 
assisted in an investigation of an apparent cluster of infant health problems 
reported among children bom to Persian Gulf War veterans in two Mississippi 
National Guard units. The medical records of all children conceived and born 
to these veterans after return from service were reviewed. The prevalence of 
birth defects, premature births, and other serious health problems appeared to 
be within range of what we would expect to see in the United States 
population. There were insufficient numbers to draw any conclusions on 
individual birth defects. Therefore, only the aggregated number of all types of 
birth defects was used. No statistically significant increases were found. 

CDC has also been asked to conduct a survey of Iowa residents to determine 
the prevalence of health problems, including adverse reproductive outcomes, 
among service men and women returning from deployment in the Persian Gulf 
We anticipate that this study will begin in early fiscal year 1995 and will 
consist of a telephone survey comparing the health status of Iowa veterans who 
served in the Persian Gulf with that of Iowa veterans who served during the 
time of the Gulf War, but who were deployed elsewhere. We will be working 
with various Federal and State agencies and veteran's organizations on the 
development of the survey protocol and the conduct of the survey. We expect 
the survey to require 24 months to complete. 



276 

As you can see, CDC has used two different epidemiologic methods for 
finding answers to questions about reproductive healtii, the case-control method 
and the cohort method. With regard to case-control studies, CDC was able to 
conduct the Vietnam Veterans Birth Defect Study in the 1980s because we 
have the oldest birth defect monitoring program in the United States, the 
Metropolitan Atlanta Congenital Defects Program, which has records on birth 
defects in all children bom in Atlanta since 1968. We were quickly able to find 
cases, match them with healthy controls, interview the parents of both groups 
to determine veteran status of the father as well as other known risk factors, 
and analyze the data to determine if Vietnam veterans' children were at higher 
risk for birth defects than other children. 

Case-control studies usually provide answers quickly, but if there is no 
registry or monitoring program, case-control studies are more difficult to 
conduct. There are three comprehensive birth defect monitoring programs 
located in the United States, in Metropolitan Atlanta, California and Iowa. 
Good monitoring programs can reveal regional differences in rates of birth 
defects and provide data to conduct studies to find causes of birth defects. 
Currently, the causes of about 75 percent of birth defects are unknown. 

In addition to the Metropolitan Atlanta birth defects monitoring program, 
CDC has recently begun a monitoring system for developmental disabilities 
which may be helpful in determining if veterans' children are at higher risk for 
conditions such as mental retardation, cerebral palsy, hearing and vision 
deficits. With regard to cancer, there are existing cancer registries, most of 
them supported by the National Cancer Institute, so that case-control studies 
could be done for cancers of the reproductive system. 

Cohort studies can also be used to examine a broad array of adverse 
reproductive outcomes. In a cohort study, one follows a large number of 
individuals for many years to determine health outcomes for them and their 
offspring. But, as in the case of CDC's Vietnam Experience study, this may be 
done in retrospect. Many adverse reproductive outcomes could be studied in 
this manner. TTiese outcomes might include premature births, low birthweight, 
and fetal deaths; developmental problems in veterans' children, such as learning 
disabilities and behavioral disorders; and morbidity and premature mortality in 
veterans and their children. 

You asked me to address a potential role for CDC in 3 areas: predeployment 
monitoring for reproductive hazards, protection during training and deployment 
of military personnel, and the assessment of reproductive dysfunction and 
abnormal birth outcomes following potential exposures. I will now address each 
of these issues individually. 

Regarding predeployment monitoring for reproductive hazards, CDC would 
be willing to work with the DOD and VA to review their current practices and 
explore if enhancements to the predeployment physical examination would be 
useful. Such enhancements might include detailed reproductive histories and the 
collection of biologic specimens, such as blood, for future assessment of 
exposure to environmental toxicants or biomarkers of disease. 

For protection during training and deployment of military personnel, CDC's 
National Institute for Occupational Safety and Health (NIOSH) could expand 
the consultation and assistance it provides DOD for addressing potential 
reproductive and other occupational health hazards. This could involve both 



277 

research to identify and evaluate potential hazards and assistance to DOD in 
developing effective disease and injury prevention measures. 

NIOSH has been providing limited assistance to DOD in reproductive health 
research since 1990. This includes consultation and laboratory (semen) 
analyses for three U.S. Army studies evaluating lead and microwave exposure 
among howitzer and radar operators at Fort Hood, Texas and Fort Sill, 
Oklahoma. These studies have not found excessive lead exposures, but the first 
study, at Fort Hood, found poor semen quality — a level associated with 
decreased fertility — among the radar operators. Since this was a very small 
study, including 21 men, it is presently being followed up with a larger study, 
the size of which is presently being determined. NIOSH is also providing 
consultation to the U.S. Airforce for a study they are conducting on the 
reproductive health of ground support troups exposed to solvents in cleaning 
jet engines. 

In addition, non-occupational issues of health protection during training and 
deployment of mihtary personnel have much in common with health protection 
in the general population. CDC, as the Nation's prevention agency, could work 
with DOD on issues of health promotion such as the consumption of the B 
vitamin folic acid by women of reproductive age for the prevention of spina 
bifida in their children. CDC could also collaborate with DOD on behavioral 
changes needed for HIV prevention, smoking cessation, violence and injury 
prevention, and many other behavioral issues related to reproductive health. 
CDC works with State and local health departments to conduct prevention 
programs of this sort and would be happy to work with DOD. 

The assessment of reproductive dysfunction and abnormal birth outcomes 
following potential exposures is something we have done for veterans in the 
past, as I have akeady mentioned, and something that we would be willing to 
do again, pending availability of resources. The studies that would need to be 
considered would be case-control studies of specific reproductive outcomes or 
a cohort study including reproductive outcomes. 

If a cohort study was considered to assess reproductive outcomes, such as 
infertility, miscarriages, and illnesses in veterans and their children, this would 
have to be evaluated and planned cooperatively with DOD, VA, and CDC. 
Based on our past experience, it should be recognized that such a study would 
be large and complex, requiring substantial resources, and would involve 
following a large number of veterans and their offspring for many years. 

Although they have geographic limitations, there are several existing birth 
defects risk factor surveillance programs which could be used to conduct a 
case-control study similar to the Vietnam Veterans Birth Defects Study. The 
Birth Defects Prevention Act of 1994 has been passed by both houses of 
Congress as a part of the Minority Health Improvement legislation and is now 
with a conference committee. This legislation authorizes CDC to assist states 
in conducting birth defect surveillance to establish registries and for CDC to 
act as a national clearinghouse for these data. If the programs authorized in this 
legislation are funded, we could determine if veterans who come from and/or 
return to specific states or regions are at higher risk than other veterans and 
non veterans. 



278 

CDC might also assist in studies of developmental disabilities in children of 
veterans and collaborate with other groups to study cancers of the reproductive 
system. 

CDC would be willing to work with DOD and VA, with their support, to 
answer these important questions which have been raised, if appropriate staff 
and funding arrangements can be made. We can provide more details on the 
possible studies which I have outlined if you wish. The promotion of health 
and the prevention of disease, disability, and premature mortality is our mission 
and it is especially important for us to do our utmost to protect the men and 
women who are protecting this Nation. 



APPENDIX 3.— STATEMENTS SUBMITTED FOR THE 
RECORD 



WRITTEN STATEMENT OF F. F GF.NF. TORONTO 

BEFORE THE 

SENATE VETERANS' AFFAIRS COMMITTEE 

ON 

REPRODUCTIVE HAZARDS & MILITARY SERVICE: WHAT ARE THE RISKS OF 
RADIATION, AGENT ORANGE, AND PERSIAN WAR EXPOSURES? 

AUGUSTS, 1994 



Thank you, Mr. Chairman and Members of the Committee. I am honored and pleased to have the 
opportunity to provide a written statement on my views and experiences regarding reproductive 
hazards and radiation exposure. 

CPL. R.F. Toronto vs. 55038062 

I was drafted on 12-2-50 and was discharged on 12-2-52. I served in the army at the Rocky 
Mountain Arsenal (RMA) for two years less three and one half mounts that were served at Camp 
Mercury located in Nevada at the Yucca Flats Atomic Test site. I now live at 10030 Girard 
Avenue South, Bloomington, Minnesota, 55431. 

I worked for Ford Motor Company in St. Paul, Minnesota for thirty years, and have been retired 
since 1983. I am now President of The Forgotten 216th, and working with my U.S. Senator, Paul 
Wellstone, a Democrat from Minnesota in regard to this issue. 

After innovation and basic training at RMA, I was assigned as a Chemical Storage Specialist and 
Spray Man Loader. Our barracks was within about one mile of a factory that produced Nerve 
(GB) Bomblets, Mustard Munition M34 Cluster bombs, also 4.2 chemical mortars, one ton 
containers of Nerve GB, Mustard and Choking agents. Nerve Agent (VX) for M-55 rockets, 4.2 
incendiaries, and smoke and slugs. As it turned out, RMA was the most polluted piece of ground 
in the worid, and was rated No. 1 on the Super Fund Clean Up list in the early 1990's. 

Our unit left RMA for Camp Mercury Yucca Flats Atomic Proving Grounds, Nevada, and arrived 
there on 3-16-52. We left our hot radiated site on 6-13-52. I was assigned on-site radiation 
monitoring into the area of Ground Zero and surrounding area. I would check out a jeep from the 
Motor Pool with another soldier, and we wouM proceed to the test site to monitor radiation from film 
badges that were attached to posts at various distances to Ground Zero. These post badges were the 
same as the badges we wore. We also had dosimeters attached to our coveralls. The same ones 
could be purchased at any clothing store. The badge and DOS/Meter were turned in at the C.P. for 
accounting of radiation we were exposed to. This did not account for the exposure we had returning 

279 



280 



to camp which was approximately eight miles or less. When approaching Ground Zero, our Ja^€^ ~ 
counters would go off scale at a max of 500 roentgens. This reading told us to depan the testing 
area. On one monitor, drive A Navy Chief and I, were included in a wind change that must have been 
very hot because when we returned to the C.P. to 5nd that j/our exposure was 3.3 or 3.4 roentgens. 
We showered and changed clothes and were back in the field the next week. 

I am now wondering if this was the right thing to do. Did the AEC know enough about the testing 
of atomic bombs to use military people in such a "NO WORRY" situation. We were told not to 
worry about radiation in one breath; and in the next breath, we were told not to reveal our job 
activities. If we did, we would be subject to stockade time, dishonorable discharge or both-- I 
wonder why?! 

After our job was over, we returned to RMA for the balance of our army stay. I was honorably 
discharged on 12-2-52. I returned home to start a family, career, and to settle down. Low and 
behoU, I was appalled to learn just a few weeks ago the army sprayed our area in Minneapolis with 
Zinc Cadmium Sulfate chemicals. Being involved with deadly chemicals at RMA, deadly radiation 
at Camp Mercury Test site in Nevada, and then living under the army spraying in 1953, 1 think it had 
something to do with the health problems in my family. When my son, who was bom in 1956, was 
32 or 33 years of age, he developed a brain imbalance. He entered into a catatonic state, lost his job 
as an insurance agent and financial planner. He also had a State Brokerage License at the time, and 
has never returned to his artkulate way of life since. He is 38 now and living at home under special 
medication. My daughter, who was bom in 1959, was and still is, struggling with a slow learning 
problem. She needed special tutoring classes in order to graduate from school, and her ability is 
limited to a job of house maid at a hotel. She is also living at home. I believe our Forgotten 216th 
was not treated in a civil humanitarian way. 

I loose a lot of sleep at night. I, myself, have skeletal problems. I had a non-cancerous tumor 
removed from between my eyes the size of a large olive pit, left side lower hernia, back siu-gery on 
the lower L4 and L5, have had my left knee replaced twice. Upon the last time replacing my knee, 
a severe infection invaded my body and no one knew why. The infection then settled in the weakest 
part of my body, the artificial left knee, which had to be removed to kill the infection. I spent seven 
weeks in bed before they were able to replace a new knee, and finally was able to see the light at the 
end of the tunnel. After arthroscopic surgery (totaling seven surgeries) on the left knee alone and 
nine months of physk;al therapy, I am able to walk again. Twelve or fourteen non-cancerous tumors 
removed, skin rash on my feet and arms, nerve ticks on my back as if bugs were crawling from my 
waist to the back of my neck and down. As of now, 1 have a lower right side hernia bulge and am 
in fear of more surgery. 

I would like at this time to thank Al-Smokey-Parish for asking me to help locate members of The 
Forgotten 216th to find out if anyone has physical or reproductive problems. We found a lot of our 
buddies have already died, leaving three widows right here in the Minneapolis area. I would also like 
to thank Senator Paul Wellstone, especially Senator Jay Rockefeller, the Senate Veterans Affairs 
Committee, and all of our officers of The Forgotten 2l6th, Robert Opseth- Vice President, Roben 
Dahl- Treasure, and Stan Johnson, who carries a tremendous load of work, and all our board 
members. I urge the Senate Veterans Affairs Committee to seriously support legislation to ensure 



281 



our government to recognize the needs of health care and other problems of atomic veterans and their 
families. I urge you to help with a federally funded study to examine the possible health and geneuc 
affects and reproductive outcomes within families of veterans who were exposed to radiation. If you 
need more information and answers, you can contact me at: 

Gene Toronto, President 
The Forgotten 216th 
10030 Girard Avenue South 
Bloomington, MN 55431 



(612) 888-3023 



Sincerely, 



Gene Toronto 
President 



GT/mt 



282 



WRITTEN STATEMENT OF LAWRENCE HIBBEN 

BEFORE THE 

SENATE VETERANS' AFFAIRS COMMITTEE 

ON 

REPRODUCTIVE HAZARDS & MILITARY SERVICE: WHAT ARE THE RISKS OF 
RADIATION, AGENT ORANGE, AND PERSIAN WAR EXPOSURES? 

AUGUST 5, 1994 



Thank you, Mr. chairman and Members of the committee. I am 
honored and pleased to have the opportunity to provide a written 
statement on my views and experiences regarding reproductive 
hazards and radiation exposure. 

My name is Lawrence Hibben and I live in Richfield, Minnesota. I 
am retired from the printing industry after 35 years working in 
color reproduction. I have been working with my U.S. senator, 
Paul wellstone (d-mn) on the issue of radiation exposure. 

From 1950 to 1952 I served in the U.S. Army, 216th Chemical 
service Co., Rocky Mountain Arsenal, Denver, Colorado, with the 
rank of P.F.C. The arsenal produced and stored weapons used in 
the Korean war including Napalm -bombs , white phosphorus bombs, 
cluster bombs, etc. Also poisonous gases such as mustard and 
nerve gas and others were also produced and stored at the arsenal 
in case they were ever needed. 

In March 1952, our company, the 216th, was ordered to report 
to camp Mercury, Nevada to witness and particpate in 8 atom bomb 
tests, our duties were varied and changed from bomb to bomb. 

I took scientists and specialists in their various fields, 
shortly after a blast, to areas close to ground zero so they 
could see how metals, fabrics, woods, etc, held up after the bomb 
was detonated. It was my job to monitor the radiation and tell 
them when they had to leave. I also flew in a plane tracking 
atmospheric radiation. I also went m shortly after a detonation 
to see how close to ground zero we could get to check how high 
the radiation was. I also monitored personnel coming in from 
contaminated areas. I also pulled duty with a civilian police 
guard at desolate outposts m the desert to make sure 
unauthorized people didn't wander into the blast area the day of 
detonation. 

I can't recall ever being told how much radiation i 
accumulated. I was in extremely high radiation areas several 
times where my instrument would go off scale — where the radiation 
was too high to read, so I had to leave the area as quickly as 
possible. The only protective clothing we had was a pair of 
ordinary coveralls (the type you buy at a clothing store). These 
were washed in soap and water and reworn. 



283 



Approximately one year after my discharge, our daughter was 
conceived, she has had life long problems with her health. At age 
14, she had numerous tumors in her breasts and had breast 
surgery. A fifth resection was done on one breast. The doctors 
wanted to perform a radical mastectomy, .but we felt such surgery 
would have been devastating on her, both physically and 
emotionally. 

At age IB she had cancer of the cervix and had kyro therapy. 
At age 28 she had major kidney surgery. Her kidney was tied to 
the back wall. The doctors didn't know why the connecting tissue 
cells dissolved. 

she has had numerous upsets with internal organs, and 
serious on-going thyroid problems, in July 1993 she was 
hospitalized for two weeks with a bowel obstruction and fed 
intraveinously because she couldn't retain liquids or solids. 
Prior to 1993 she was hospitalized 4 years in a row. Her doctor 
says her whole system went out of "whack" and couldn't explain 
why. Three months ago she was tested for a lump in her neck and 
was told to watch it. 

The doctors have never been able to answer our questions as 
to why her health is so poor. 

My daughter's son, now 17, was born with feet deformity. His 
heels were displaced, and his arches were inverted. He spent the 
first 5 months of his life with casts on both feet up to the 
knees. He has had a serious skin condition for years that does 
not seem to respond to normal medications. 

In searching for an answer to all her problems, my daughter 
asked if her mother had been on any medications, or anything 
else, during pregnancy, that could have been harmful to an unborn 
child. My wife took excellent care of herself. 

we always wanted to have more children and waiting years 
with no results, we tried to adopt a child, since we already had 
one child we had to go for fertility tests in 1958. My wife 
checked out fine, but they found that I had an uncommonly 
enlarged prostate gland that was severely infected and I had an 
extremely low sperm count. I was told I had been fortunate to 
have fathered one child and most likely would never father 
another. I was put on medication and after numerous office calls 
was told the condition was chronic and most unusual for a young 
man 29 years old. I doctored with this uroligist until he retired 
in 1985. Now I see the doctors at Group Health, we never had any 
more biological children. 

AS events unfolded during my life, I didn't give any thought 
about linking all the radiation i ingested and accumulated in my 
body with having something to do with the way things turned out. 

As a young, trusting soldier, I believed the Atomic Energy 
Commission knew what they were doing and were truly concerned and 
looking out for my health and welfare. Now I honestly believe we 
were used without enough regard for our health and well being. 

we served in good faith, putting our trust in the hands of 
people who assured us there was nothing to be afraid of, or worry 
about. 

The truth is, these atomic tests we were subjected to took 
place less than 7 years after Hiroshima and Nagasaki. There 



284 



couldn't possibly have been any data on long term effects of 
radiation, or for that matter, what constituted "quote-unquote" 
safe radiation dosages. 

I understand that some downwind civilians have already been 
compensated for radiation damages, shouldn't we who had to live 
and work near the bomb sites for 3 months be considered for 
compensation, some of my buddies have died, others, with serious 
health problems have been denied treatment at veterans Hospital. 

Mr. chairman and committee Members. I want to thank you for 
taking this issue seriously. I urge Committee Members to support 
and craft legislation to ensure that our government recognizes 
and responds to the health care needs of atomic veterans and 
their families. I urge committee Members to support a federally 
funded study be commissioned to examine the possible health and 
genetic affects and pregnancy outcomes within families of 
veterans exposed to radiation. 

THANK YOU 

If needed, I would be pleased to provide you with additional 
information and to answer any of your questions. Please contact 

me : 



Lawrence Hibben 
6309 Logan Avenue so 
Richfield, MN 55423 
(612) 869-1939 



Thank you, again 



285 



WRITTEN STATEMENT OF DR. WALTER FUNMAKER 

BEFORE THE 

SENATE VETERANS' AFFAIRS COMMITTEE 

ON 

REPRODUCTIVE HAZARDS AND MILITARY SERVICE: WHAT ARE THE RISKS OF 
RADIATION, AGENT ORANGE, AND THE PERSIAN WAR EXPERIENCES? 

AUGUST 5, 1994 



Thank you, Mr. Chairman and members of the committee. I am 
honored and pleased to have the opportunity to provide a written 
statement on my views and experiences regarding reproductive 
hazards and radiation exposure. 

My name is Walter FunmeJcer and I live in Minneapolis, Minnesota 
where I am married to a beautiful women, Linda and we have six 
children who are being raised to believe that life is wonderful. 
I have used the G.I. bill to achieve my B.A. degree and I am 
grateful to the U.S. government for this opportunity. Currently, 
I eun working as a cultural anthropologist at a university and my 
research training has been useful in the creation of an Atomic 
Survivor database, starting with the Lake Mead Base, Las Vegas, 
Nevada contingent of which I was a member as a marine guard. The 
question of the Atomic Veterans and the impact of radiation has 
had on these veterans and their families is an issue which will 
not go away despite the attrition that radiation has had already 
on thousands of needless American veterans death of which I will 
be one. I have been working with my U.S. Senator, The Honorable 
Paul Wellstone (D-MN) , on this issue because he cares about the 
regular people of this country who helped defend this land where 
life is sacred. 

I volunteered for the United States Marine Corp for a three year 
enlistment in 1953 from a small town in western Wisconsin called, 
called Black River Falls. I thought I was fullfilling my service 
obligations to the United States of America. I went through boot 
camp at Marine Corp Recruit Depot, Platoon 486, in San Diego, 
California. I, then took advance Infantry Training at Tent Camp 
Two, after finishing, I was assigned to the 7th Marines at Camp 
Las Pulgas, Camp Pendleton, CA. I asked for Korea duty but I was 
turned down to become part of The Lake Mead Base contingent. I 
was assigned Military Police duties while waiting to be given 
security clearance. I spent eleven months at Lake Mead base. Las 
Vegas, Nevada where nuclear weapons were assembled and stored to 
be used at the Tonopah Navy gunnery range located on an American 



83-529 95-10 



Indian reservation, which later became Camp Desert Rock and the 
nuclear test site. In the eleven months of duty I observed six 
nuclear events which had an unappreciated physical and 
pyschological impact on me. At that time, my government reassured 
me, through officers that nuclear weapons were safe and our 
rentgen gauges would alert us to danger levels. I did not realize 
that the rentgen gauges were limited and did not measure over 
premeasured limits of the gauges. I became fearful of the fallout 
and I had no knowledge that I was infected with radiation. I was 
reassigned back to Camp Pendleton where I was honorably 
discharged in 1956. 

There were a number of Native Americans who were in the Lake Mead 
base contingent but I don't know how many are alive today. 
I am a member of the Wisconsin Winnebago tribe who have signed 
twenty two treaties with the U.S. government regarding our 
landbase and we have fought against the U.S. government to retain 
our sovereignty. I, as a Bear Clan warrior, come from a long line 
of warriors who have used fear as an ally. Winnebago Warriors 
have fought not only in the Indian campaigns but in the major 
wars as well. Although, the Winnebago Tribe has been reduced to 
five thousand people through govermental attrition, from a once, 
one hundred thousand population to the present numbers. The 
Winnebago veterans have won all the war honors that this 
government gives from medals of honor to many purple hearts. The 
Winnebago Warrior has always fought for Mother Earth while the 
native born American has fought for the flag. 

I have been married three times because I have wanted children. 
My first wife, whom I had known during 1954 had two miscarrages 
and became sterile. We seen medical doctors who tried to help but 
it was too difficult to have children because, at that date, we 
didn't know the culprit to be radiation. 

My second wife had one miscarriage but out of the union we had a 
son. It was a difficult pregnancy for her and after the pregnancy 
her ability to become pregnant disappear completely. Again it was 
radiation that lead to her infertility. 

My third wife, who was young and able to conceive had two 
miscarriages, but because of her youth, she went on to have six 
children. We watch our children very close for any radiation 
related illnesses. There is a lot upper respirtory illnesses and 
asthma among them. 

I was very sick during the early 1980 's and posed a lot of burden 
on my young family. I became destitute because I ran out of 
health insurance and had no job because I was sick. I finally 
went to V.A. hospital and was admitted because of my 
classification as an atomic veteran. I am now have out-patient 
status and in a very weak state of health. 



287 



My recommendations for the Committee members is to take this 
radiation sickness seriously for the American survivors, just as 
seriously as the research on Japanese survivors where we spent a 
lot of American tax dollars and none for our own veterans. 

I urge committee members to support and craft legislation to 
ensure that our government recognizes and responds to the health 
care and other needs of atomic veterans and their families. 

I urge committee members to support a federally funded study be 
commissioned (not by duplicity) to examine the possible health 
and genetic affects and pregnancy outcomes within the family of 
veterans exposed to radiation. The survivors and the descendents 
need to compensated for the unseeable and unknown genetic 
destroyer call radiation sickness. That free radical that has 
infected all exposed people to radiation sickness. 

Walter Funmaker 
1026 112th Ave. S.E. 
Minneapolis, Minnesota. 55414 
612/ 331-6083 

Thank you, again. 



288 



WRITTEN STATEMENT OF HILMAR MAYERHOFER 

BEFORE THE 

SENATE VETERANS' AFFAIRS COMMITTEE 

ON 

REPRODUCTIVE HAZARDS S MILITARY SERVICE: 

WHAT ARE THE RISKS OF RADIATION, AGENT 

ORANGE AND PERSIAN WAR EXPOSURES? 

AUGUST 5, 1994 

Thank you, Mr. Chairman and members of the Committee. I am honored and pleased 
to have the opportunity to provide a written statement on my views and experiences 
regarding reproductive hazards and radiation exposure. 

My name is Hilmar Mayerhofer. I live in Shakopee , Minnesota. I am now retired 
- formerly worked as a machinist. I have been working with our United States 
Senator, Paul, Wellstone (D MN . ) on this important issue. 

I was in the United States Army Chemical Corps in 1950 to 1952. I was a RFC 
and stationed at Rocky Mountsdn Arsenal in Denver, Colorado. I was sent to 
Mercury, Nevada, where I was an offsight monitor for three (3) atomic tests and an 
onsight monitor for five (5) atomic tests. X was exposed to 2900 MR on record 
through a film badge (That is what I was told'.) However, film badges were not 
issued at all times and I was most likely exposed to much higher radiation as were 
many others at the test sights. We had no special protective clothing, we used 
our gieger counters to check radiation. No one knows how accurate those were. For 
a short period of time, my giegercounter read 20R which was the highest reading I 
ever had at the test sight. We were never allowed to discuss radiation after we 
got out of the service. This was considered classified information. 

I really think that some of the medical problems we've had over the years could 
very well be linked to radiation exposure. Especially, since discussing the 
similar problems with other men who were at the test sights with me. We have three 
(3) living children but we lost three (3) babies due to premature birth. All three 



289 



only lived a few hours each. Our youngest living son has a mental illness, paranoid 
schizophr/enia. He also was born prematurely. I believe there is a correlation be- 
tween our reproductive problems and radiation exposure. 

I want to thank the Committee members for studying these issues. I would 
sincerely hope that there be some legislation put forth that would insure that our 
government respond favorably to the health care and needs of all atomic veterans. 
Please support a federally-funded study to examine the possible health and genetic 
effects on veterans and their children exposed to ratiation. 

If needed, I would provide you with additional information regarding the before- 
mentioned medical problems. You may contact me at (612) 445-2382 or 

Hilmar Mayerhofer 
781 South Jefferson 
Shakopee, UN. 55379. 



Thank you again. 



Sincerely, 



HILMAR MAYERHOFER 
781 South Jefferson 
Shakopee, MN . 55379 



290 



Mr. James R. Gerararig 
7141 Redwood Hwy. 
Grants Pass, OR 97527 
Phone: (503) 474-7332 



August 24, 1994 



Dr. Patricia Olsen or Dr. Diana Zuckerman 
Senate Committee on Veterans Affairs SR 414 
Russell Senate Office Building 
Washington, D.C. 20515-6375 

Dear Dr. Olsen or Dr. ZucJcerman: 

I am one of the thousands of veterans who served at Japan in 
1945 to 1946. I joined the Marine Corps on June 4, 1945, and after 
basic training, was sent to Gueun and then to Nagasaki, Japan as 
occupation troops. I served there until the Marines were sent home 
or to other bases. No one told us that we were in any danger from 
the bombs after effect s and were only told to not drink Japanese 
water. 

I have been to the bomb site many times on guard duty, touring 
the area, and living with a Japanese family while off duty. I 
drank their water, ate their food, swam in the reservoir, and in 
general was a part of the population for eight months. 

I helped the family rebuild their house with materials I took 
from the bomb area. Their home was on the other side of a mountain 
from the main bombed out area, so their house was lived in "as it 
was" for months because there were no materials to fix it. I did 
not mind being in Japan or blaune the government for sending me 
there. I only wanted to be treated for my cancers. 

In 1946 late to 1947, I was in Tientsin, China, when bumps on 
my arms were removed surgically by a Dr. William B. Fetters. He 
had me assigned as an ambulance driver during this time. He never 
told me if they were cancerous or not, and maybe he did not know 
because he was only the base doctor. 

Later in life in the 1950 's as a civilian, I had more bumps 
removed and the doctors said they were cysts. I got married and 
during a five year period, my wife lost four babies through 
miscarriages. One was from having measles during her pregnancy, 
but the other three, the doctor could not explain. She did not 
know why my wife lost three children. 

I served as a policeman from 1950 to 1979 and during this time 
I had supposed "cysts" removed from both ears, on my face, 
forehead, and arms. 

After retirement, I joined the Second Marine Division 
Association to see if I could find some of my old Marine buddies 
and I found one who told me he had cancer and that his doctor had 
told him it was due to his exposure in Japan. I wrote a letter to 
the Defense Nuclear Agency and to the Veterans Affairs to get a 
check up at a V.A. hospital. 



291 



Dr. Olsen or Dr. Zuckerman 
August 24, 1994 
Page 2. 



They told me to get an appointment at the V.A. Hospital in 
Long Beach, California. This hospital would not see me until I got 
an okay from the Veterans Affairs. Next they said I had to file a 
claim and prove that I was in the Nagasaki Occupation Troops. I 
had my service record sent to me and found that my health record 
had no mention of the bumps taken off my arms. The Dept. of 
Veterans Affairs did finally admit that I was in Nagasaki, Japan, 
but my claim was denied. 

I filed again to get to a V.A. Hospital and more paperwork and 
again my claim was denied, because I could not prove the bumps and 
cysts removed were cancerous. I had another growth developing on 
my arm but had no health insurance, was in bad finances, so I 
neglected it. 

I moved to Oregon and again filed to get this cancer removed 
from my arm explaining it was there for a doctor to see. Again I 
was denied. I had the cancer removed, had a biopsy done on the 
thing, and it was cancerous. I sent the letter from my doctor 
explaining what it was, and that it was caused by the radiation, 
and now the V.A. has put my case on hold because of their work 
load. I don't think I asked for too much, only to have my cemcers 
removed by a V.A. Hospital, but I had to pay to get them out 
instead . 

It seems funny to me that our government can spend billions in 
foreign aid, spend billions to fight wars for other people, and 
then import the boat people, Cubans, Haitians, etc., but can't 
afford to take off my service related cancers. Something is rotten 
in Denmark, when we don't take care of our own servicemen, when the 
government put us in harms way in the first place. 

I currently have additional cancer which needs to be removed. 
I would appreciate any efforts you can make on my behalf to get 
through the bureaucracy of paperwork, overloaded work schedules, 
etc. and allow me to be seen and treated in a V.A. Hospital. 

Thank you for your time and your efforts on my behalf. 

Sincerely, 



James R. Gemmrig 
JRG:bg 



292 



u=« . 1 d L. bmeltzer 
448 Easb dBOO bouth 
Sandv, Utah 84070 
801-561-1387 

Written Testimonv for Public Hearina 

Committee on Veterans Affairs 

United States Senate 

Reproductive Hazards and Military Service, August 5, 1994 

Senator Jay Rockefeller 

414 Russell Senate Office Building 

Washington, D.C. 20510 

Dear Sirs: 

I am writing this letter in regards to the hearings that »re 
or have taken place on the genetic effects on children of 
veterans who were exposed to ionising radiation. 1 am one of 
those children, and my mother at this time has a claim pending 
locally in Pittsburgh, on behalf of mv father who died of cancer 
of the kidneys on April 2, 1993. 

My father was assigned to a unit of the United States Navy 
known as Cub 18, Navy No. 3912, (also known as Lion 9> , which was 
a supply outfit attached to the Third Marine Division. He was 
stationed in Sasebo, Japan from early October 1945 until July 
18th. 1946. During this time he was involved with supplying and 
taking CAre of the Third Marine Division, and was allowed to 
travel and go to Nagasaki which was very near by without any 
dangers or restrictions being made aware to him. His doctor of 
twenty years has written the VA that in his professional opinion 
this exposure was the cause of his early demise. 

That then brings us to mvsel f . I was born January 23, 1953 
in Pittsburgh, Pennsylvania. My mother took no drugs or 
medications whatsoever during her pregnancy. She was not exposed 
to any hazardous materials as well. Mv father never had any 
exposure to hazardous materials in his employment with the phone 
company, only that exposure to radiation in Nagasaki. I was born 
with a congenital birth defect known as bilateral svndactylism 
with complete webbing between the 4th and 5th fingers on both 
hands. The distal phalanges and the actual bony phalanges were 
fused bilaterally between the distal bony segments. This 
condition had never existed in our family of any sort going bacJ 
four generations, and came as a complete surprise and shock to 
both sides of our familv. 

Tfiis defect was corrected at a voung age with several 
revisions as 1 grew older. We never made any connection to it and 
my father s exposure until the early eighties when the effects ot 
exposure started to be made known. Even then the defect had been 
corrected and I had a fairly normal life. Then in the early 
eighties I started to have problems walking. 1 was turned down 
because of physical problems with my legs for several promotions 
that reguired physical ability to climb telephone poles. At first 
my doctor tested for arthritis and I tested positive to having a 



293 



positive rheumatoid factor. So for many years I went along 
thinking my increased walking difficulty was due to rheumatoid 
arthri tis. 

After being laid oii fr-om the telephone company I was hired 
by the State o-f Utah as a Driver License Examiner in 1989- After 
about 8 months on the job I was again experiencing problems with 
my legs, due to being required to be on my feet a great deal of 
the day. Upon suggestion of a friend 1 sought out an orthopedic 
surgeon who had prescribed arch supports for her son who had 
juvenile arthritis. When the doctor picked up my foot he 
immediately found what they call a non sustained ankle clonus, 
and sent me to a neurologist. Upon his examination it was 
determined that I had lost approximately 50% of the use of my 
lower limbs, and had spastic paraparesis. I was sent for an tIRI, 
which showed large sections of the myelin in the brain were 
missing. The neurologist took several weeks to decipher the MRI 
because neither he nor the radiologists had ever seen anything 
like it. They told me there was nothing they could do and told me 
to come back in a year for a follow up. 

We were lucky enough that summer to see a report on a 
disease called ALD. that was associated with the Odone s of 
Lorenzo s Oil fame. They're description of the MRI sounded much 
like mine. We contacted NBC, got the Odone s number and were then 
refereed to Doctor Hugo Moser at Johns Hopkins University. I 
thought at last we may have at least found an answer to what was 
going on. 

Upon talking to Dr. Moser I was told that his lab could run 
a series of tests that could determine if I had ALD or various 
other Leukodystrophies. He asked if I would mind working with a 
Dr. J. Richard Barinoer at the University of Utah, which I did. 
After running the tests twice because of negative results it was 
concluded that this did not explain my condition even though the 
MRI looked like it should. 

Dr. Baringer then ran tests for every known similar 
neurological problem all to no avail. It was then concluded that 
there was no known origin for my disease. However they could tell 
me that it would be progressive, and degenerative, and they could 
not tell how fast it might advance. 

I am now 41 years old. I am no longer able to work and I am 
on Lotal disability. I have lost the normal use of my bladder, 
and sexual function. I suffer from vertigo attacks, and extreme 
fatigue. The prognosis is still the same. 

This year we have become aware that the birth defect that I 
was born with is being associated with abnormal white matter 
diseases of the brain similar to mine. It is a svndrome called 
the oculodentodigital dysplasia syndrome, and I do fit it. I have 
also found that I have another birth defect of a malrotated 
intestinal track which places my appendix on my left side and not 
my right. 

The scary part of all of this is that I have 5 out of ^ 
children that also have the same congenital defect, who are 
probably looking at the same neurological consequences. 

I have attached a' copy of an article on the svndrome from 
1''90 out of the University of Pennsylvania. I am sorrv that I do 



294 



not have an original copy. 

Mv father I feel has definitely e.:posed, while in Nagasaki. 
He returned with sever dvsenterv. having vomiting, sever -fatigue, 
sever diarrhea, and nausea. I believe this was actually radiation 
sickness. His exposure then leads to our family s now continuing 
sever health problems and will probably continue for generations. 

I hope that my information may be of help in the hearings 
that are taking place. If further information is necessary please 
feel free to contact me. I will be more than happy to share with 
anyone what has occurred in our family, 

I know that I am not alone and that there are many others 
who are also suffering. Many of those who are may not even know 
that they're medically unexpl ainabl e conditions have an 
expl anation. 

Ironically my disease's symptoms are very similar to those 
Gulf War Vets that were exposed to depleted uranium. Hence 
leading me to believe that exposure can alter genetically, and 
cause this sort of problem. 

1 will be anxiously awaiting your reply to my information, 
and again hope it will be of use. 



Sincerely, 



CLw^<?^ 



David L. Smeltzer 




295 



0^ 



American Journal of Medical Genetics 41:18-20 (1991) 



Oculodentodigital Dysplasia Syndrome Associated 
With Abnormal Cerebral White Matter 



Daadd-I I . C ul m a nn, EUlne H. Zackai, Donna M. McDonald-McGinn. Kenneth H. FUchbeck . 
and John Kamholz 

Tht Department of Nturol<^fy. The Hospital of the Uniueriity of Pennsylvania (DJi.C, KJHF.. JX.), 
and Tht Division of Clinical Gtntties. Childrtns Hospital of Philadelphia (EJi2., DMMJ, Philadelphia, 
Penntyiuania 



OeulodentodlgiUl dysplasia (OODD) syn^ 
drome Is sn uncommon inherited disorder 
with eye and facial abnormalities, syndactyly, 
and defects in tooth enamel. Some of the pre- 
viously reported patients with ODDD syn- 
drome also manifested spastic quadriparesis. 
We describe a patient with sporadic ODDD 
syndrome referred for evaluation of progres- 
sive spastic paraparesis. Magnetic resonance 
imaging of the brain demonstrated abnormal 
white matter, which suggests an explanation 
for the observed spastic paraparesis. 

KEY WORDS: hereditary spastic parapare- 
sis, leukodystrophy 



INTRODUCTION 

Oculodentodigital dysplasia (ODDD) syndrome was 
originally reported in the (}ermsn literature in 1920 
IMcKuiiek 16420; McKusick. 19881. AfTected patienU 
manifest: 1) bilateral microcornea, sometimes sssoci- 
ated with iris anomalies and glaucoma: 2) syndactyly 
of thi .'ourth :nd nfl.'i fingirs; 3) facial 8Hior»p.sIities 
with small nassl alae snd anteverted nostrils; snd 4) de- 
fects in dental enamel (Dudgeon snd Chisholm, 1974; 
Gillespie, 1964; Gorlin et al., 1963; Ragic and de Veber, 
1966; Sugar et al., 1966). In some of the reports, affected 



individuals manifested spa stie ps rapsreais or quadri- 
j^aresls, hyper*^exia and gait dilTIculties I Barnard et 
al., Igglr Belghnwf tt al.. 1979: Reisner et al.. 1969: 



Niv eion-i;nevall ier>Wil~, 1981 1. This Trnding was often 
attributed IB eervlCII fUllJ lUiiipieMion due to vertebral 
hyperostosis, although this was not consistently docu- 
mented by myelography, plain films of the cervical 
spine, or pathologic study. We report on a patient with 
aporadic ODOD syndrome who exhibits spsstie para- 



i April 27. 1990: July II. 1990. 

I to Dr. Divid It. Gulmiinn, it hin pm- 
tnt addrcM Th« HowsH Huxhn Medicsl InitituK. 4570 Mcdksl 
Scisncs RcsMnh Buildinf It, Tlit University of Michigan, Ann 
Arbar, MI 48109. 

O 1990 Wiley-Uas, Inc. 



paresis and white matter abnormalities on brain mag- 
netic resonance imaging (MRt). This finding msy pro- 
vide an explanation for the spastic paraparesis in our 
patient as well as in previously reported eases of spastic 
paraparesis. 

CLINICAL REPORT 

A 21-year-old right handed woman nursing student 
was referred for evaluation of clumsiness while walking. 
She was the product of a normal pregnancy, gestation, 
and delivery. There was no history of intrauterine X-ray 
or other teratogenic exposure. In childhood, she wsa 
noted to have short toes, syndactyly of the 4th and 6th 
fingers bilaterally, microcornea, and a markedly de- 
prMsed nasal bridge with bilateral epicanthus (Fig. 1). 
Subsequent X-ray studies showed aplasia of the middle 
phalanges of the toes bilaterally. 

In high school, she had dental films that demon- 
strated severe enamel hypoplasia. At that time she 
noted that she would trip frequently while wslking, snd 
by age 20, she could not walk long distances without 
tripping or losing her balance. She was recently evslu- 
ated by her family physician and found to have a normal 
computerized tomography (CT) scan of the brain, nor- 
ms! thjToid functic." tssta, and undet^tsble anti- 
nuclear antibody and latex agglutination rheumatoid 
factor antibody levels. Cerebrospinal fluid analysis did 
not contain white blood cells, protein level was 39 mg/dl, 
glucose 60 mg/dl, VDRL was nonreactive, and it con- 
tained normal immunoglobulin G levels, normal myelin 
basic protein levels, and nooligoclonal bands on protein 
electrophore!iis. Visual evoked and brainstem auditory 
evoked potentials were abnormally prolonged, suggest- 
ing white matter dijieRse. Visual acuity was 20/20 and 
rcd-grccn color vision by Ishihara color pinte testing wss 
normni in both eyes. There was no family history for 
ODDD, neurological deficits, or facial anomalies. Th* 
mother hnd two accond trimester miscarriages before 
the birth of the patient The patient had one full-sib and 
three half-sisters (two with the same mother and one 
with the same father), as well as six nieces and neph"«J 
who are all unaffected. The mother was 29 years old .nnd 
the father was 43 years old at the time of the patient 5 
birth. 



296 



OODD and Cerebral Leukodyitrophy 



19 




Fif. I. Patient with OODD lyndnHn* at arte S. Tha charattn-iatk 
acta* nndlnn af mkrtxnnMa. dramaed naaal bridfa with bilateral 
■ trtafcrtam aa wall " ' * ' 



I arndactyly at th* 



Phyiieal examination or tiie patient showed micro- 
oomeae (8 mm), small nasal alae, anteverted nostrils, 
repaired syndactyly of the 4th and eth Hngera bilat- 
erally, absence of the middle phalanges of the toes, and 
yellow discolored teeth. Although she appeared to have 
hypertelorisin, the interpupillary distance was on the 



80th centile. Neurological examination demonstrated 
spastic paraparesis, lower limb hyperrenexia, nonsus- 
tained ankle clonus, pronounced scissoring of gait, and 
extensor renponses to plantar stimulation. She appeared 
to have normal intelligence and received good grades in 
nursing school. There was no evidence for glaucoma, 
scoliosis, or sensory disturbances. Dental films demon- 
strated severe enamel hypoplasia. MRI of the brain 
demonstrated diffusely abnormal high signal in subcor- 
tical white matter extending inferiorly to the medulla, 
and abnormal iron deposition in the thalamus, basal 
ganglia, and gray matter of the temporoparietal gyri 
bilaterally (Fig. 2). MRI of the cervical cord was normal 
with no evidence of cord compression. Biochemical eval- 
uation for the known leukodystrophy syndromes showed 
normal levels of very long chain fatty acids (ad- 
renolcukodystrophy), arylsulfatase A (metachromatic 
leuI:ody9trophy), and ccrsmide 3 galactosidase (globoid 
cell leukodystrophy). Plasma amino acids, urine organic 
acids, hexosaminida.^e A and B, and human T-cell leuke- 
mia virus-! (HTLV-I) antibodies were normal. Chromo- 
somes were normal (46, XX). 

DISCUSSION 

The finding of abnormal CNS white matter by evoked 
potential and MRI evaluation may provide an explana- 
tion for the observed lower limb spasticity in our patient 
as well as in previously described cases. Reisner et al. 
11969) described a mother and her 7V»-year-old daugh- 
ter with ODDD syndrome who manifested weakness 
and bilateral ankle clonus in the lower limbs with gait 




' Imaslnii 61 the brain In (hr patient with 01)1)11 ■ 

■ ii«h fiiiinal inleniily in Ihe aubcsrtical while matter bilal- 
vl (Al aa compared la a nsrmal erte-mauhed brain (Bl. Imaxea were (enerated on a 1 .6 IMa 
111 rUt - 90; TV - 3.0001. 



297 



Gutmann et aJ. 



ataxia and dyametria on nn^r-to-no8« and heel-to-skin 
testing. The other children of this mother had ODDD 
syndrome without neurological abnormalities. No ex- 
planation waa provided for thia obaervation. Beighton et 
al. (1979) described two patienta with ODDD syndrome 
and upper motor neuron dysfunction. One male had 
serere spastic quadriparesia with acleroaia and hyper- 
oatoaia of the cranial vault and baae. An unrelated male 
developed progreaaive gait difTiculty beginning at age 6, 
requiring a wheelchair at age 16. He had spaatic quadri- 
pareaia and poaitive Babinski reflexes. CT scan demon- 
strated calciHcation of the baaal ganglia without white 
matter abnormalitiea. Theae authors attributed the 
apaatic quadriparesis to apinal cord compression from 
presumed hyperostosis at the base of the sku ■!. Nivelon- 
Chevallier et al. (1981] described a case of ODDD syn- 
drome with spastic paraplegia that they could not aa- 
cribe to hyperoateeia and spinal cord compre.^sion, as BarpafS A. lUmenun* 
myelography waa normal. The father of thin 36-yenr-old^'-'^"';' ?"'5'"*""^ ' 
man also had ODDD syndrome and difTiculty walking. "" «»^'**-'"*^ 

but a paternal grandfather had ODDD ayndrome and no 
gait abnormalitiea. TWo casea of ODDD syndrome were 
described by Barnard et al. 11981] with severe spastic 
quadriparesia and basal ganglia calciHcationa. My- 
elography performed on one patient demonatrated cervi- 
cal cord atrophy without evidence of cord compresaion. 
The clinical and radiographic featurea were similar to 
those observed in our patient. 

The ODDD syndrome occurs aporadically or as an au- 
toaomal dominant diaorder IMcKuaick 16420; Mc- 
Kuaick 1988). There is one report of preaumed autoao- 
mal recessive inheritance (IVaboulski et al., 1986). 
Some sporadic casea ariaing from new mutetiona have 
been aaaociated with advanced paternal age, aa waa the 
caae in our patient [Jonea et al., 1976). Baaed on the 
prea e nce or abaence of aasociateid spastic paraparesis 
and cerebral white matter abnormalities, the phenotype 
of ODDD ayndrome should be expanded to include spas- 
tic paraparesis. The presence of families with some aiba 
manifeating ODDD syndrome plus apaatic paraparesie 
and aome manifeating only ODDD ayndrome arguea for 
variable expreaaivity of the rtsponaible gtne, as see in 
neurofibromatosis type 1 jRiccsrdi and Lewis, 1988). We 
recommend that all caaeaof ODDD syndrome be studied 
by brain MRI to further investigate the relationahip 
reported herein. F\iturc reaearch ahould provide in- 



sighte not only into genes involved in the production ar 
maintenance of central nervoua ayatem myelin but ah 
genes that regulate morphogenesis. 

ACKNOWLEDGMENTS 
We thank Dr. David Pleaaure for referring this paticr 
to ua. Dr. Michelle Williama for reviewing the denti 
films, the metabolism laboratory at the Children's Ho 
pitel of Philadelphia for helpful discussions, and D 
Hugo Moser (Baltimore, MD) for analysis of the ver 
long chain fatty acids. We appreciated the help of M 
Deniae Marie Lalli in preparation of this manuscrip 
Thia work waa supported in part by National Institute 
of Health Program Project grant NS08075 in Neurt 
muacular Diaeases (Dra. Kamholz and Fiachbeck). 

REFERENCES 

H. 



BclftiUm P. IUm«rmn« H. Riwd M (I979h OcukMienl»H»M«ut djripl 

lia: h«t«ref tneity or T«ri«bl« oprwton? Clin G«t>et 16:169-17 
DudK«en J. ChiiMm lA (1974): 0«uled«fitadinUl drnlMia. IVar 

Ophthalmol Sac UK 94:203-210. 
i« FD (19S4): A hendiUrr n 
tiUli*.' Arch Ophthalmol 7I:lS7-in. 
Oorlin RJ. Mnhin Ul. St Omt JW (1963): Oeabdnladifiul drapl 

•ia. J Ptdiatr «3«9-78. 
Jonn KU Smith DW. Ilarrty MAS. Hall BO, Quan L (1975h OM. 

paternal art* and frnh (an* muUiiaa: daU an additional diaordtr 

J Ptdiatr 86:84-88. 
McKuakk VA (1988): -Mtndtlian InheriUnc* In Man: CataloRi 

Autaaemal Dominant, Aotoaemal Rcttniv* and X-Uniitd Ph 

notypn.' Eighth adition. BalUmarcTh* Jehna Hopkins Univenii< 

Nlvden-Owvallier A. Aadr; D. Andry F, DumM R (1981): Djrspla 
• oeultf dmie-diyitala. A prapoa d'lm eu a**c paraplcfi* apatn 
U-tflquc. J Genet Hum 29:171-179. /^(vfi'fi 



, Relt»«f SB. Kott e, Bomatein B, Salinfftr H. Kaplan I. Gorlin I 
W^1969): Ocalod*ntadi|«Ul draplaala. Am J Dia Child 1 18:600-6<> 
Rlceardl VM. Ltwia RA (19881: Fy«ctrancc of *on Rnklinnhau- 



danU. Am J Human C«n«t 42:284-289. 
Suxar HS. Thempaen JP, Davii JM (1966): The oculedcntodifiul d 

plaaia ayndremc. Am J Ophthalmol 61:1448-1481. 
IVaboulakl EI. Faria BM. DerKalouaUan VM (1980): renittent h>i 



298 



Melanie Ayers Gulf War Babies 

6729 Pin Oak Lane PO Box 25446 

Fayetteville UC 28314 FayeCteville NC 28314 
(910) 867 7751 

6th August 1994 

Dear Senator Rockefeller, 

I have just returned from attending the hearings held on 
Friday August 5th regarding the reproductive hazards of military 
service where we heard the statements of various people 
concerning their own stories as well as the scientists opinions. 

Firstly, I would like to thank both you and your staff for 
putting these hearings together and giving us all a voice. As 
difficult as it was to hear some of the personal testimonies it 
was something that was very much needed and obviously long 
overdue . 

I don't know how much you know about my case, however, I 
understand that Diana Zuckerman may have filled you in a little 
as you so graciously acknowledged my work during the hearings. I 
had hoped to testify but I understand that time was a little on 
the short side. I have enclosed a copy of the testimony I so 
desperately wanted give and I hope that you can find the time to 
glance at it. The mother of the little boy named Matthew that I 
mention in ray testimony managed to grab a moment with you after 
the hearings came to an end. (I myself was busy moving my car to 
avoid getting it towed and returned to find that everything was 
over. ) 

From what the other ladies told me you managed to grill the 
lady from the Dept . of Veterans Affairs. Upon returning home I 
read through the copy of her statement . On page 5 she states that 
only 1.6% of children conceived after service in South West Asia 
were born with birth defects according to the figures taken from 
the Persian Gulf Registry. I would like to bring it to your 
attention that every time either I myself or any of the other 
families, who's children are either sick or who have died, but 
the actual service member is not sick themselves (as is the case 
with all of our group), have tried to register, there has been 
nowhere to record us in their computer! In fact, there are a 
number of families who, because they are not sick themselves, 
think that their child' s problems or their spouses constant 
miscarriages could not be related to the Gulf War and therefore 
are not registering. It is presumed that the service member would 
have to be sick first. Because of this, the Registry could not 
possibly reveal the true statistics and until a full survey is 
done of all Gulf War Veterans as opposed to just those who have 
heard of the registry, the true statistics will never be known. 
Of course, we are all very aware of how easily a statistic can be 
manipulated too. It is a standing joke amongst our group of 
calling up the hotline or the offices of the local registry and 



299 



always hearing the same thing, "Oh, hang on a moment, I'm not 
sure where to put you on my computer!' 

Once again, I would like to thank-you for your time and for 
believing us when no one else seems to want to. For those of us 
who's children are dead, it is a relief not to have someone 
patronize us and presume that in our deep grief we must have 
flipped our lids to think such things could be happening! I'm 
sure you would be surprised to know that that is exactly how all 
of the doctors have been treating us so far. . .we must be going 
through the 'anger stage' of our grief; it'll pass, just humor 
them until it does! 

I have enclosed a photograph of our son Michael taken just a 
few days before he died. I think that everyone assumes that these 
children look deformed and therefore that it is probably a 
blessing that they are no longer with us. I ask you, does this 
little boy look like he's going to die suddenly to you? None of 
these children were given a choice, most of them, once born, 
aren't even getting a chance. I'm hoping that this picture will 
give you one more little face to a name and help you to know that 
all of your hard work is worth it. No one should ever have to go 
through what we are all living daily! 

I hope that I can continue to keep in contact with you and 
your staff. If I can be of any further assistance at anytime 
please do not hesitate to let me know. 

Sincerely yours. 



Melanie Ayers. 



300 



Melanie Ayers Gulf War Babies 

6729 Pin Oak Lane PO Box 25446 

Fayetteville NC 28314 Fayetteville NC 28314 
(910) 867 7751 

This is our son Michael. God blessed us with him June 1st of 
last year. Michael's first cry completed, what was for us, the 
perfect family. We had already been blessed with a beautiful 
daughter who had been born the day the Gulf War started and 
although her Daddy had not been present at her birth nor 
witnessed the first innocent months of her life, all of that 
seemed a long way behind us as we finally shared the moment of 
our childs first cry together. 

It was a very hot and humid summer in North Carolina, 
something I believed explained Michaels constant and profuse 
sweating problem. But as the summer passed and turned to Autumn I 
became concerned when it not only didn't improve but seemed to be 
getting worse. Michael was permanently soaked. 

At his four month well baby check-up it was noted that 
Michael wasn't gaining enough weight and was very quickly sliding 
towards the bottom of the weight chart. The doctor didn't show 
particular concern for this problem and attributed his sweating 
to him just being a 'hot boy*. 

Just four weeks later we all attended a children's halloween 
party at a friends house. Whilst there we met a family who also 
had an older girl and a little boy Matthew and we struck up the 
customary mothers chit chat . 

That party proved to be our last family outing. On the night 
of November 3rd Michael didn't seem to be himself and wasn't 
interested in feeding. It took until past midnight to get him 
settled. At around 3.30am he awoke with a pitiful cry. I held him 
close and just rocked him quietly. Within minutes he began to 
look lethargic. Gradually his breathing became labored and noisy. 
I awoke my husband and the decision was made to take him to the 
hospital. Just after I backed out of the driveway he stopped 
breathing, his head fell forward and he died. The CPR performed 
by my husband, the rescue squad and the hospital was to no avail 
and he was officially pronounced him dead at 5.30am. 

An autopsy revealed massive undetected heart defects in the 
form of two extremely rare diseases. His heart had gradually 
become enormous and misshapen due to a mitral valve deformity 
present from birth. In our grief the questions came unceasingly. 
How could this happen, why did it happen and how could a child 
die with something so terribly wrong with him and no one have 
known . 

In the months that followed I casually came into contact 
with other families who had -also lost a child. A couple who's 
little boy had been still born with umbilical cord defects, a 



301 



baby who had been born with the left side of her heart not 
functioning who lived two short days, another little boy who 
survived for just thirty-eight days with a mitral valve defect, 
all who had one thing in common - their fathers had all served in 
the Gulf. I learned that three neighbors had experienced six 
miscarriages between them and I heard of yet emother childs 
death. Once again, all of these children were Gulf War Babies. I 
became alarmed. In my pursuit of answers to Michaels death I read 
endless articles and reports on the frequency and criteria of 
infant mortality. During all of this research I received a call 
one day from a friend. Did I remember Matthew the little boy from 
the halloween party? His mother had found him dead in his crib 
that morning just 4 1/2 months after Michaels death. His autopsy 
revealed that he had died from undetected primary cancer of the 
liver, a disease more frequently associated with older men who 
have consumed large quantities of alcohol. I was very shaken; 
Matthew was yet another Gulf War Baby. 

All of these children came from well educated, middle 
class families with excellent health habits who had received 
medical care from the day they discovered that they were 
pregnant. We are all married, in our twenties to early thirties 
and live in good housing conditions thus putting us ALL outside 
of the list of factors normally considered to influence infant 
mortality. It just didn't make sense to me. 

I then learned of yet two more cases of infants stillborn to 
Gulf War Veterans, one of which had very extensive birth 
defects. One morning I met a lady in the PX. Her son had no arms 
and only hands attached to his shoulders. We struck up a 
conversation and I learned that her husband had also been in the 
Gulf. I later learned that Jayce suffers from a rare heart 
disorder which carries along with it the absence of his arms. 

A member of the staff at the local civilian hospital 
obstetrics unit told me of the noticeable increase among military 
patients coming into the unit in pre-term labor at 26 and 27 
weeks gestation and loosing their babies . 

When we lost Michael we were told that it was just 'one of 
those things'. Well the one thing that links us all together is 
the fact that one or sometimes two of these childrens parents 
served in the Persian Gulf. 

I and the mothers of some of the other children that I have 
mentioned have made this journey here today to bring this tragic 
situation to your attention and to put some faces behind the 
stories. It has been nine months and one day since Michael died. 
In that time new lives have been created and these precious 
children are being born as we speak. Yet nothing has been done to 
follow these pregnancies a little closer. Since our children died 
nobody has tested either us or our husbands for anything. No one 
wants to listen to our fears of having more children, and we have 
come to terms with the fact that our children cannot be 



302 



registered on any of the Persian Gulf War registries. Just where 
do you register someone who is already dead? 

Coming here and speaking to you all today is one of the last 
things that I can do for Michael as his mother. I'm hoping that 
it may even help to save the life of at least one other child. 

This will always be Michael. I ask you to look into these 
blue eyes and realize that you have a responsibility to him and 
all of the other innocent children of the men and women who serve 
this country, to end this shameful and tragic tradition. 

Thank-you for your time. 



303 



Kim S Sullivan 

9 Markham Street 

Fort Bragg NC 28307 

(910) 497 2066 5 August 1994 

Sadly, on March 26, 1994, just a little over four months 
ago, our seemingly healthy 10 month old son, Matthew, died in his 
sleep during the night. Unless you have lost a child of your own, 
you probably cannot imagine the tremendous amount of pain this 
loss has dealt to our family. We are having a terribly hard time 
understanding it ourselves. 

After a carefree evening of play on the family room floor, 
on Friday March 25th, I put our son. Matt, to bed as usual. I 
thank God that we did spend the last evening of his short life 
playing. You see Matthew was just starting to walk, just starting 
to enjoy playing and just starting to keep up with his big 
sister, Emily. 

What was so unusual about this weekend was that the next 

morning after our play session, I walked into our sons room to 

find him dead in his crib. No symptoms, no warnings, hopefully no 
suffering. 

We spent the next few hours in a hospital Emergency Room 
waiting for a doctor to confirm what we already knew, that our 
son was dead. Now that shock had set in, we had to wait for an 
autopsy report. What a terrible procedure to put a little body 
through. As a Criminal Justice graduate and having to view an 
autopsy in my studies, I have always vowed I would never put 
anyone I loved through that process. And suddenly I was waiting 
for the autopsy report of my ten month old son. SIDS or Sudden 
Infant Death Syndrome seemed to be the most logical answer at the 
time, even though ten months is normally over the age range for 
that condition. And in the back of ray mind I wondered had Matt 
choked to death on something that had gone unnoticed in his 
mouth, and if so, how could I handle the guilt? So you can 
imagine the shock we felt, as on Monday morning the Medical 
Examiner gave to me the cause of Matthew's death, which was 
Heptoblastoma or a primary, malignant, liver cancer. Actually the 
tumor had ruptured and our son had hemorrhaged and eventually 
went into shock and died. All this while I slept in the room 
beside him and had earlier thanked God for my wonderful children. 

I realize that daily, children are diagnosed with cancer, 
but my research shows that liver cancer in infants is less than 
two cases per million, and that the symptoms surface at about age 
three. This cancer killed my son, with no symptoms, at age ten 
months. Not only is liver cancer in infants unusually rare, it 
seems unlikely to be hereditary. And there are no cases of this 
cancer in our families history. Research has also shown that 
certain chemical and environmental exposures can cause 
chromosomal damage that can be transmitted through paternal germ 
cells to the infant. The liver functions much like a filter to 



304 



eliminate the impurities of the body, leaving it's immune system 
weak in an already immature infant body. 

Because of the recent media attention given to Gulf War 
exposures and because of the oddity of our sons death, we cannot 
help but wonder if there could be a connection between these. 
Since Matthew's death we have talked with many families who have 
suffered the loss of a child and the one issue that keeps 
surfacing is that all of the fathers are Desert Storm Veterans. 

Since my husband is active duty Army and since we reside on 
a military installation, those resources are the channels through 
which we have pursued any physical tests that could hopefully 
rule out our fears. In the four months since our sons death, and 
after repeated requests for any blood or semen analysis, or any 
genetics studies, we have been told only that there is nothing 
that can be done. 

We do not know if Desert Storm exposures had any 
relationship to Matthew's cancer, nor will we ever know unless 
someone is willing to help us find some answers. We need these 
answers for the sake of our next child, yet to be conceived. And 
for other families like ours. 

We are fortunate that we have a beautiful, four year old 
daughter, named Emily, whom by the way was born before Operation 
Desert Shield/Storm. Finally, please understand that we are not 
asking anyone to try to compensate for our loss, that would not 
be possible. But what is possible is that a series of tests could 
enable us to continue on with a normal life. 

Thank-you very much, 

Kim Sullivan. 



305 




/V) /AJu)/yi (J- j^oL, /:6in(.m : 






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306 







307 



lAugusU994 
To Wboai it may concern. 

fbave been requested bv Sgt Sieve Miller to ivrite a statement oa any Jjiowkc^e 
or experiences f bave bad concerning birth anomalies or defects tbatbave occurred 
witi members of our Armed Forces folio wing Operation Desert Shield/Desert 
Storm. 

It was ivith reluctance Sgt miller asked me to write thisasfaa still on Active 
Duty and be expressed great concern because of possible reprisals botb subtle and 
noi-so-subtle tbat could occur, to me . witb tin's statement 

Folio wing my deployment to Southwest Asia I was re-ass^nedto Brook Army 
Medical Center where my duties included working in the Neonatal Intensive Care 
Unit Over a period of approximately a year and a half I noticed an increase in the 
number of babies bom with various bMi defects. This was also confamed by other 
Health Care providers and nursing personnel who had been stationed at this 
location far a number of years. In every case involving Active Duty parents, either 
one ex- both had been assigned to a [fniiin the Fersian Gulf during Desert 
Shield/Deserl Storm. 

Although the direct cause of these birth defecis is not known it appears to 
canrelate highly with the fad these unfortunate infants had parents who were 
deployed to the Fersian Gulf prior to then- conception. 



^Uavid S Smith 



Sgt. USA 



308 



MAJOB BICBABD B. BAIHES 
U.S. ABMT BKSEBVK 
REFOBT TO THE OOMOBESS: 4247 VALLEY TEBBACX 

HEN ALBANY. IMDLMiA 47150 
QOLF NAB BABIES TELE 812 948 9366 

THEY ABE CHBONICALLY ILL.~A pilot survey of ttaa babies of Qulf Nar Veterans 
has found them chronically ill with increased Incidence of premature death. 
This finding runs counter to the recent Mississippi Health Dept/CDC study 
sayintf Gulf War babies were within population norms. They have admitted 
publicly that their statistics tabulated only overt deformities, not chronic 
respiratory or asthma problems, nor reactivity to baby formula, foods, and 
medications. This convenient omission ocourred after they found widespread 
respiratory problems. Afain, American health leaders have turned their back 
on the plight of Qulf War Veteran families. I ask the Congress to stop 
pretending, to stop deferring to ixtdustry-paid consultants abusing VA/DoD 
authority to sustain the ooverup and to start soma real homework on the 
medical reality of multiple ofaemical s ena ltivity. long ago recognised by the 
Social Security AdministratioB and by BOD. 

87X OF 33 NBITTEN BBSFOMSES SBOHBD ASTBMA <» BBACTIVITT.— In a written 
symptoms survey of 33, 32 (97%) evidenced ofaronic arthma problems or 
reactivity to baby formula, adults foods, medioatione and household cleaners. 
20 (61%) evidenced manifestations of imaune depression as manifested by 
sustained flu-like oonditioos despite antibiotics, as well are repeated ear 
inflammations. Some of the babies have actually been diagnosed immune 
depressed. Eleven (33%) evidenced slowed growth, underdeveoped motor skills, 
and poor muscle tone, most of which were demonstrated by those babies with 
deformities. 

These baby tabulations were not drawn from a statiatioally representative 
segment of afflicted Vets, but they were all from babies conceived since the 
Gulf from either a father or mother (usually the father) who did serve in the 
Qulf. The findings are unique in that the abnormalities are disproportion- 
ately unique, even for a self-named pool of afflicted babies. 

The combination of constipation and diarrhea within a 24 hour period for 
a baby is indicative of food reactivity, according to leading environmental 
pediatricians. When these repeatedly occur following the consumption of 
certain foods and medications, then food and chemical reactivity is in fact 
suspect. In some cases, the babies experienced immediate restrictive airway 
and related symptoms when they were exposed to recently treated carpet or 
a household oleaner. 

THE SYMPTOMS POINT TO MDLTIPLE (BEMICAL SENSITIVITY. — The trend line is that 
the babies of the Qulf Vets have multiple chemical sensitivity and I believe 
they do. As they age beyond the first year, they are Increasingly exposed to 
low level toxics outside the safety of their crib — they crawl on pesticide- 
treated lawns, are vulnerable to freshly painted rooms and interiors, play 
with plastic toys and objects and often put them in their mouth, and they 
begin to consume an increasing variety of adult foods. As they do so, their 
respiratory and asthma-like conditions and chemical reactivity. 

The medical reality we see unfolding with Gulf War Syndrome runs counter to 
the previous testimony and public statements of Joshua Lederberg, MD, of the 
Defense Science Board to wfaiofa I testified in February hearings at the 
Pentagon. The Defense Science Board is a premier civilian advisory group 
to the Dept. and to the Congress, and Dr. Lederberg' s assumptions, I believe, 
are part of what are public policy inertia that is keeping our soldiers sick. 



I publicly challenge Lederbertf's statemen-ts that chemical hypersensitivity 
"are learned". Many of these Qulf War babies are now reactive to low level 
toxics, and I'd like to know how in the beck a one-year old "learns" to be 
reactive to carpet treatments and household cleaners. I'd like to know how 
these babies "learn" repeated constipation and diarrhea after consuming a 
wide range of baby formulas, medications, and adult foods. A true scientific 
review of the Gulf War babies would have counted all miscarriages, abortions 
due to deformity, premature deaths, aa well as chronic illness. 

A telephone survey of 96 Gulf Vet families from all sources showed 11 babies 
had died from complicated health problems and that from among the 85 who 
remain alive, 27 (32X) have experienced deformities. The deformities 
statistic is not deemed representative of all Qulf Vets, but I point out 
that the reason some of the deformed babies are now excluded from government 
statistics is because they're already dead! 

These findings are also being made available to the Association for Birth 
Defective Children in Orlando. \rt)icb is immediately launching a nonclinical 
study of Gulf War babies. Ask for Betty Mekdeei at 407 629 1466. 

INFORMAL PILOT SORVEY OF 33 UBITTEM RBSFONSSS OH SYMPTOMS. — 

Ear inflammation or fluid buildup 66X Adjacent are the percentage of 

Repeated diarrhea S8X incidence of 33 written surveys 

Perspires a lot SeX noting abnormal symptomology. 
Persistent oolds despite antibiotics 58X 

Asthmatic/respiratory problems 55X Outraged Veteran families are 

Frequent vomiting 55X appealing to the American public 

Runny nose or stuffiness 55X with a series of fund-raisers 

Drools a lot 48X commencing immediately. 

Awakes at night without cause 4SX 

Abnormal rashes 42X All three networks and many 

Scratches ears excessively 42X major metres and magazines are 

Slowed physical & motor development 39X currently developing stories on 

Arches back when sucks bottle 36X the baby crisis. Hollywood is 

rectal gas 33X working on docu-dramas. 

Nasal stuffiness when on bottle 30X 

Socks and bangs head excessively 30X Even those elected officials 
Frequent hiccups during gestation 30X purporting to be actively 
Buttocks have appeared scalded 30X investigating the issue, fail in 
Problems falling asleep 27% their surveys to take note of 
Sneezes a lot 27% acquired chemical sensitivities, 
Scratches scalp often 27X which Vets experience repeatedly 
Allergic to baby formula 24X when around home and work low- 
Often makes clucking sounds w/bottle 24X level toxics. The disablement. 
Poor muscle tone 24X hospitalizations, bankrupticies 
Often has red ears 24X will hit taxpayers to the tune 
Slowed reflexes 15X of over $1 million apiece for 

these 100,000 afflicted families 

Private donations and commitments in support of Gulf War Vets from the 
private sector now total over $50,000 and are growing rapidly. It is 
apparent that the Congress has failed in it's leadership to address the 
affliction of over 100,000 Veteran families. It continues its failure to 
conduct an epidemiological study, to test the Vets for obvious toxics, and to 
systematically review brain impairment, immune depression, and damaged 
central nervous systems. This failure continues because Congressional 
staffers are not doing their homework, «ure not learning about the tests and 
diagnostics for this illness, are not cross-examining VA/DoD/CDC in their 
mis-statements, their equivocations, and their statistical Frankensteins. 



310 



6DLF WAB A^TEBANS BABY LIST 8/24/94 

THIS LIST IS BESEABCH AND PROPEBTY OF MAJOR BICHABD H. BAIMES 

FOR BABY SOBVEY INFO. CALL 812 948 9366 OB HBITE 4247 VALLEY TEBBACE 

NEN ALBANY, INDIANA 47150 

PARENT INFO BABY INFO 



SPRINGDALE, MO 72762 

FR. IS SENSITIZED TO BLEACH 

AND SOLVENTS. 



MOLLY BETH, BORN 5/9/94. DOWN' S SYNDROME 
HAS HAD 12 DIFF. DR'S. AV HEART DEFECT. 
12 DIFF DR'S. AB CANAL DEFORMITY. 



M.A. 

DENVER, CO 80231 



BRAIN OF 13 MO BABY STOPPED DEVELOPING. 
BABY DIED. 



T & K 

BARRINGTON, XL 60010 

FR SENSITIZED TO CLEANERS, 

SMOKE AND PESTICIDES. 

FATHER WAS ACTIVE DUTY. 



ALEXANDER. DOB 1/20/93 DEFORMED, AS IS 
CURRENT PREGNANCY. ALSO HAD MISCARRIAGE. 
ALEXANDER HAD LUNG, HEARING AND VISION 
PROBLEMS, PLUS PERSISTENT COUGH , WHEEZ ING 
ALEX HAS PERSISTENT COLDS, DESPITE 
ANTIBIOTICS, AND $2 MILLION HOSP. BILLS. 
ANTIBIOTICS, CALCIUM DEPOSIT IN KIDNEYS. 
PREGNANT WITH 2ND DEFORMED BABY WITH 
ALTERED HEART, EXTRA DIGITS. AND POSSIBLE 
ASSYMETRICAL HEAD. 



M.A. 

DENVER. CO 80224 



PREMATURE BABY-BRAIN NOT DEVELOPING 
DIED 6 MO OLD. BABY HAD NIGHT SWEATS. 



A & M 

TUCSON. AZ. 



MISCABBIAiGE. HAVING TROUBLE CONCEIVING. 



J & M 

E AMHERST. NEW YORK 14015 



CODY, 5/29/93. PERSISTENT ASTHMATIC. 
PERSISTENT COLDS. ASTHMA TREATMENT 
DIDN'T HELP. CONSTANT WHEEZING. REACTIVE 
TO MEDICATIONS. EAR INFLAMMATIONS. 



B.A. 

CLINTON, MD 30735 



BABY ALLEBGICALLY REACTED TO ANTIOBIOTIC 
2 POST-GULF INFANTS IN FAMILY. 



K & A 

TAFT, CALIF 93268 



SHANIA. 12/28/93. CTR OF BRAIN MISSING. 
DEFORMED TOES. TON OF OTHER PROB. 
NO CORPUS COLLUSUM. CROOKED TOES. REFLUX 
& FREQ SEIZURES. BODY IS STIFF & UNCOORD 
REPEATED EAR INFLAMMATION. FREQ. SNEEZING 
HEARING PROBLEMS AND CROOKED TOES. 



FAYETTEVILLE, N.C. 28314 
FATHER WAS ACTIVE DUTY. 



MICHAEL. DOB JUNE 1. 1993. CONGESTIVE 
HEART FAILURE—MUCH OVERSIZED HEART. 
PERSPIRED A LOT. BODY WT STEADILY DECL 
BABY DECEASED. 



311 



G & K 

COLT NECK, NJ 07722 
MOTHER SENSITIZED TO 
SOME HOUSEHOLD CLEANERS. 
FR. WAS ACTIVE DUTY. 



HOLLY, DOB 5/22/92. 2 KIDNEY INFECTIONS. 
SLEEP APNEA MONITOR FOR 15 MO. ASTHMA & 
RESPIRATORY PROB. AND WHEEZING, SNEEZING. 
EAR INFLAMMATIONS. SLOWED MOTOR DEVEL. 
QUIT BREATH WHEN 2 1/2 HRS. OLD. REACTIVE 
TO SEVERAL BABY FORMULAS. 



JACKSON, MS 39203 

MOTHER WAS ACTIVE DUTY AND 

RECORDS 18 SYMPTOMS. 



DWAYNE DOB 2/17/92. CHRONIC EAR PROB. 
CHRONIC BRONCHITIS. TAKING BREATHING 
TREATMENTS. DEFORMED UMBILICAL CORD. 
RESPIRATORY/WHEEZING. EXCESSIVE DIARRHEA 
VOMITING, CONGESTION, AND CONSTIPATION. 



R.A.B. 
BILOXI, MS 



2 YR OLD BABY BOY WITH MISSING LEFT 
EYE, CLEFT PALATE, MALFORMED LEFT EAR, 
MALFORMED NOSE, 2536 OF BRAIN MISSING, 
RESPIRATORY PROBLEMS, IMPAIRED HEARING, 
BORN WITH PART OF BRAIN IN HIS MOUTH. 



A.B. 

LOUISVILLE. KY 40216 



2 PREMATURE BABIES, JACORIE REACTIVE TO 
BABY FORMULA— ALSO HAS RESPIRATORY AND 
OTHER PROBLEMS. 



P & L 

FAYETTEVILLE, NC 28314 
MOTHER WAS ACTIVE DUTY AND 
IS REACTIVE TO CLEANERS 



GRACE, DOB 1/27/94. REACTIVE TO MILK. 
3 OPEN HEART SURGURIES. LEFT SIDE OF 
HEART IS UNDEVELOPED. EXCESSIVE SNEEZI 
COLIC. 



S & D 

SAN ANTONIO, TX 78233 

FATHER HAD ELEVATED RADIATION, 

AND PNEMONIA 4 TIMES PAST 2 YRS. 



KENNEDY, 2 YRS HOLD, MISSING THYROID. 
PROBLEMS WITH FORMULA, SWITCHED TO SOY. 
HYPERSENSITIVE TO PENICILLIN. EGGS, MILK. 
3 LASER SURGIERS ON THROAT. RASHES ON 
FACE. 



S & L 

JUNCTION CITY, KS 



2 MISCARRIAGES. 



B & A 

VIRGINIA BEACH, VA 23464 
BOTH PARENTS ACTIVE DUTY IN GULF. 
FR. REACTIVE TO EXHAUST, CLEANERS, 
AND CIGARETTES. FR. HAS 21 SYMPTOMS 
MOTHER HAS 15 SYMPTOMS. 



RYAN: 1/12/92. CYST ON SPINAL CORD. 
URINARY TRACT DISORDER. 9 OPTNS. NATURAL 
FATHER, AGED 25, DIED OF ILLNESS. RYAN 
IS ALLERGIC TO SOME MEDICATIONS. SPIKING 
FEVERS. 13 PTNS AS OF AUG. 1, '94. 



S.C. 

CAMBRIDGE, NY 12816 



13 MO OLD W/ ABNORMAL HEARTBEAT. BABY GIRL 
URINARY TRACT INFECTIONS. 



VALRICO, FL 33594 



MICHAEL. II. 1/31/93. DIED 8 MO OLD. 
AUTOPSY: LACERATED ORGANS. 39 SYMPTOMS 



312 



J & J 

TACOMA, WASH. 98443 

BOTH PARENTS WERE ACTIVE DUTY. 

MOTHER HAS 18 SYMPTOMS. 



BRETT, 2 YRS OLD, REPEATED IMMUNODEF 
ANTIBIOTICS WON'T HELP. BABY NOT 
ABSORBING IRON. PLACENTA SEPARATED EARLY 
ASTHMA AND RESTRICTIVE AIRWAY. PNEMONIA 



EXCESSIVE DIARRHEA AND EAR INFLAMMATION 
PERSISTENT COUGH. VOMITING PHLEGM. 



W i M 

LAUREL. MS 39440 



8/8/93 WILLIAM HAS CONSTIPATION, NAUSEA, 
WHEEZING, EXCESSIVE VOMITING. VOMITS 
CLEAR PHLEGM, NEARLY CHOKING. REACTIVE 
TO MOST BABY FORMULA. SOY i GOATS MILK. 
REACTIVE TO CLNRS PINESOL AND MR. CLEAN. 



L 8c P 

MANHATTAN, KS 66502 

FATHER SENSITIZED TO BLEACH. 

AIR FRESHENERS, DIESEL, SOLVENTS, 

EXHAUST AND CIGARETTES. FR HAS 

19 SYMPTOMS AND WAS ACTIVE DUTY. 



BLAKE RYAN; JULY 23. 93. HYDROCEPHALOS . 
EAR PROB. SLOWED GROWTH. COLIC. DIARRHEA 
AND VOMITING. RASHES AROUND EYES. POOR 
MUSCLE TONE. 



M.D. 
SUMMERTOWN, 



MAURICE, 5/24/93: STGRANGE RASHES. 



D.D. 

ST. PAUL, MN 55109 



BABY DAUGHTER, APPARENTLY W/MCS. 
2 SINUS SURGERIES. 



D & P 

NEW ALBANY, 



BABY NEARLY DIED WITH COLON PROB. SEVERE 
NITESWEATS, IRRITATED EYES, DRY SKIN. 



J & D 

WINDSOR LOCKS. 



2 YR OLD DEFORMED BABY. 
WITH PANCREATIC CANCER. 



FATHER TERMINAL 



LAUREL. MS 39440 



JONATHAN HAS ALLERGIES. WHEEZING, 
PERSISTENT COLDS DESPITE ANTIBIOTICS. 
ABNORMAL VOMITING AND CONSTIPATION. 



J.E. 

WYLIE, TX 75098 

FR. DIAGNOSED WITH HODGKINS LYMPHOMA. 



JORDAN. 12/10/93. RESPIRATORY PROBLEMS. 
ALLEGED CONSTIPATION & DIARRHEA. 



S & P 

HAMTRAMCK, MI 48212 

BOTH PARENTS ILL. 



NATHAN, 2/26/92. POSSIBLE SLOWED GROWTH 
AND UNEXPLAINED, REPEATED RASHES ON NECK 
AND FEET. LITTLE INT. IN FOOD. 



EAST LANSING, MI 48823 

FR. WAS ACTIVE DUTY AND IS 

REACTIVE TO CHEMICALS & FUMES. 



BRITTA, 2/26/92 WITH ABNORMAL 
BACTERIA AS FOLLOWS: KLEDSIELLA 
PNEOMONIAE; NUMEROUS NON-HEMOLITIC. 
RARE COAG-NEG STAFF. ALSO ALPHA STAFF. 
TYPE BACTERIAL. BABY HIGHLY REACTIVE TO 
CHEMICALS. 



313 



C 8c L. 

LAKEWORTH, FL 33463 



BLAKE, BORN W/ TRACULA MALAYSIA. HAS 3 
NIPPLES. 



CHARLOTTE. NC 28205 



BABY ALLEGEDLY ILL. 



J & M 

THE COLONY. TX 75056 



RYAN 9/11/92. 2 MO PREMATURE . OTHER PROB. 



D & J 

LINDEN, AL 36748 

BOTH PARENTS ILL. 

FATHER SENSITIVE TO CHEMICALS. 



KELSEY. 12/4/92. EXCESSIVE DIARRHEA. 
RESPIRATORY PROB AND RASHES. PROBABLE 
REACTIVITY TO FOODS. 



J & M 

LAKE FOREST. CAL 92630 



HAD TO ABORT DUE TO SKELTAL DYSPLASIA 
(UNDERSIZED BRAIN). ALSO SHORTENED LIMBS 
BELL SHAPED RIBS. CAULIFLOWER-SHAPED HEAD 



J & K 

GRAND PRAIRIE. TX 97051 



BABY DAUGHTER'S FORMULA HAD TO BE 
ALLEGRA. 



OGDEN, UTAH 84405 



3 MISCARRIAGES. 



R. G. 

SAVANNAH. GA 31401 



BABY DIED IN CRIB FROM ABNORMAL ILLNESS 
FATHER CHARGED W/MURDER 



R & P 

LADOGA. IN 47954 



JAKE: 6/24/93 16 SYMPTOMS. 

BABY TAKEN AWAY BY ST. PROTECTIVE AGCY. 



COLONIAL HEIGHTS. VA 23834 



MISCARRIAGE 



M.H. 

KILLEEN, TX 76S541 



TWO-YEAR OLD BABY BABY ALLEGLY IS 
CHRONICALLY ILL. 



P & C 

FT. BRAGG, N.C. 28307 



BABY DEFORMITY WITH HANDS AT SHOULDERS 
AND NO ARMS. 



M & E 

ROGERS, ARK 72756 

FATHER WAS ACTIVE DUTY AND 

RPTS 55 SYMPTOMS. 



JOHN 'BLADE" DOB OCT. 2, 92. BREATHING 
ATTACKS. BABY HAS 15 SYMPTOMS, PLUS 
REACTIVITY TO STRONG CLEANERS. 



C.H. 

NEWARK, N.Y. 07103 



MISCARRIAGE 



SALT LAKE CITY. UT 84119 



314 



JORDAN. SICK BABY. 



& D 
TERRELL, 



HAVE SICK BABY 



D & S 

WEST GERMANY 

ACTIVE DUTY PARENTS 



DAUGHTER BORN WITH HOLE IN HEART. 



LOWELL. ARK 72745 

FATHER AS AEROBIC DEFICIENCY 

SINCE THE GULF WAR. 



FORCED TERMINATION OF PREGNANCY, DUE TO 
NUMEROUS DEFORMITIES, INVOLVING EXTRA 
FLUID ON SIDE OF BRAIN. BABY WAS DEEMED 
HAVE VISION AND HEARING PROB.ALSO SEVERE 
CLEFT PALATE. MISSHAPENED HEAD. 



HUTCHINSON, KS 67501 
MOTHER HAS 16 SYMPTOMS. 
18 SYMPTOMS. 



AMBER, DOB: 1/11/94. RESPIRATORY, HOSP 
2 WKS, REACTIVE TO AMMONIA. CHRONIC 
DIARRHEA AND VOMITING. REACTIVE TO MILK 
REACTIVE TO SIMILAC. WHEEZING. 



E & J 

NORDRIDGE, VA 22192 

WAS ACTIVE DUTY. 



ERIC, 2 YRS OLD W/SEVERE CLEFT PALATE 
OTHER SURGERIES. 



T.K. 

LAVISTA, NEBR 68128 



DAKOTA (HE) DOB 12/18/93. 
REACTIVE TO MOLDS. 



DIFF SIZED EAR 



CAMP LEJEUNE, N.C. 28542 
FR. HAS 12 SYMPTOMS. 



BYRON, JR: 2/29/94. RESPIRATORY AND 
PERSISTENT COLDS, DESPITE ANTIBIOTICS. 
12 SYMPTOMS 



OSKHOSH, 



MIKAELA. 1/20/94. CLEFT PALATE i LIP. 
EAR INFECTIONS. 



J & K 

PORTAGE, IN 49002 



2 POSTGULF YOUNGSTERS WITH RASHES 



N & K 

POWDER SPRINGS, GA 30073 

BOTH PARENTS SENSITIZED & SICK. 



TROY HAS EXCESSIVE DIRRHEA, EAR INFECT- 
IONS. SNEEZING AND STUFFINESS, VOMITING 
FUNGAL RASHES. KELLY HAS ASTHMA AND 
WHEEZING, EAR INFLAMMATIONS. HEADACHES. 



R i L 

COLUMBUS. GA 31909 



SAMUEL HAS SLOWED DEVELOPMENT. SEIZURES. 
12/27/91 IS DOB. DIAGNOSED AUTISTIC. 
ALLERGIC TO YEASTS. 



815 



MAYFIELD. UTAH 86643 



BABY ALLEGEDLY ILL. 



M & D 

CHEYENNE, WY 80007 



MICHAEL JR. SEPT. 22, 1993. RESPIRATORY 
PR0B. PERSISTENT COLDS DESPITE ANTIBIO. 



K & J 

HATTIESBURG, MS 39402 



PETER RYAN: 4/18/92 HAS DISCOLORATION 
ON HEAD AN ABDOMEN. TOUCHED, THEY 
WELL UP AND TURN RED. EAR PROB AND 
ALLERGIC TO MEDICATIONS. 



A & H 

OCEANO, CA 93445 



L3 WK OLD FETUS DIED. + 2 MISCARRIAGES. 



M & S 

CAPE MAINE. NJ 08204 



MISCARRIAGE. NEWBORN. DILLAN. 11/22/92. 
HAS WHEEZING PROB SINCE BORN. 



S & T 

SOSO, MS 39480 



1/17/92 JOSEPHA HAS WHEEZING. DIGESTION 
PROBLEMS, EAR PROBLEMS. EXCESSIVE SPIT. 
PARENTS BOTH NOW CHEM. SENSITIVE. BABY 
HAS PERSISTENT COLDS DESPITE ANTIBIOTIC 



D.L. 

SEFFNER. FL 33584 



ALEX HAS HEMOPHILIA. (A)=CLASSIC FACTOR 
VIII-SEVERE DEFICIENCY. ALSO ASTHMA. 
NO HISTORY OF HEMOPHILIA IN FAMILY. 



E & T 

BENSALEM. PA 19020 

FR. WAS ACTIVE DUTY 



TERRIBLE EAR INFECTIONS. ALLERGIC TO 
A MEDICATION. UNEXPLAINED RASH. 
JAUNCICED WHEN BORN. 



G & T 

DANAPOINT, CALIF. 92629 



5/3/94. CHRONIC RESPIRATORY PROBLEMS AND 
EAR AND RASH PROBLEMS 



R & L 

JACKSONVILLE, NC 28546 



SEVERE ANENCEPHALY (ABSENCE OF PART OR 
ALL OF THE BRAIN AND UPPER SKULL). 
DIED 8 HRS AFTER BIRTH. 



T.M. 

PEARLINGTON, MS 39572 



1ST BABY BORN WITH UMBILICAL CORD 
TWISTED AND AMNIOTIC FLUID WAS 
CEUSPARATING (SP?). HAD TO TAKE 2ND 
BABY TWO MONTHS EARLY-ON HEART MONITOR 



D & T 

LAWRENCEBURG, IN 47025 



SEVERE HEART AND JAUNDICE PROBLEMS 



316 



D & T 

LISBON, OH 44432 
FATHER WAS ACTIVE DUTY MARINE. 
SENSITIZED TO MANY CHEMICALS. 
MOTHER HAS 42 SYMPTOMS. 



DESIREE,DOB-6/14/93. FREQ. COLDS. 
FEET PEELING IN BIG LAYERS. RASHES. 
MONTH-LONG RASHES. EXCESSIVE VOMITING, 
DIARRHEA, ASTHMA AND RESPIRATORY PROB. 
EXCESSIVE SNEEZING, CONSTIPATION. 



T i L 

WAYNESBORO, MS 39367 



1/24/93 ANTHONY HAS ALLERGIES AND 
WHEEZING AND HAD TO USE GOAT'S, NOT COW 
MILK. ABNORMAL AMT OF VOMITING AND 
DOUBLECHECK ON DEFORMITY. REACTIVE TO 
SYNTHETICS. 7 DAYS SPEC HOSPITALIZATIONS 
21 SYMPTOMS. 



K & S 

WILSONVILLE, ALA 35 If 



SONOGRAM SHOWED TWINS NOT DEVELOPING 
NORMALLY AND WERE ABORTED. 



TOPSHAM. ME 04086 



JACOB. DOB 10/16/93. BRONCHIAL BLOCKAGE. 
ASTHMATIC, RESPIRATORY PROBL. WHEEZING & 
FREQUENT VOMITING. DROOLS A LOT. A 2ND 
CHILD WITH POSSIBLE PROBLEMS. 



T «t J 

COLORADO SPRINGS, CO 80911 



2 MISCARRIAGES. 2) NEWBORNS. BILLY HAS 
CHRONIC INFECTIONS AND EAR INFLAMMATION. 



T & M 

CHICAGO RIDGE, IL 60415 



MICROCEPHALY (BRAIN AND SKULL UNDER- 
SIZED). CEREBELLUM UNDERDEVELOPED. 
AMANDA 1/18/94 



H & A 

WAYNESBORO. MISS 39367 
FATHER WAS ACTIVE DUTY AND IS 
SENSITIZED. BOTH PARENTS ILL. 



JOSHUA LEE WITH DOB: 2/3/92. DAMAGED IMMUNE 
TAKING BENEDRIL. REACTS TO BALONY AND 
HOT DOGS AND HOUSEHOLD CLEANERS. REACTIVE 
TO FOODS. SPIKING FEVERS. ASTHMA AND 
WHEEZING. SUSTAINED RASHES ALL OVER BODY 
ALLERGIC TO DISPOSABLE DIAPERS. REACTS 
BUG BITES, FLIES, MOSQUITOS, WHICH DON'T 
HEAL. 



S & B 

SAN ANTONIO, TX 78217 



CEDRICK, 3/1/92, HAS 3 DEFORMITIES. 
COLDS WORSE THAN REST OF FAMILY. 



B & M 

FT. MEAD, MD 20755 



CASEY DOB; 8/7/93. UNDERDEV. ESOPHOGUS. 
DIAG. W/GOLDEN HAR. DEFORMED EARS. 
JAW IS DEFORMED. FACE IS CROOKED. 
8 SURGERIES ALREADY. 



M & L 

HOWELL, MI 48843 



RESPIRATORY PROB. WITH TWO CHILDREN, 
MELISSA & MEGHAN. WHEEZING. 



83-529 95-11 



317 



D & R 

HOPEMILLS. HC. 28348 



MATHEW. 5/7/93. MAJOR RESPIRATORY PROB.i 
ASTHMA. TUMOR BEHIND TRACHEA. 



D M 

PORT ISLAND. LA 70767 



MISCARRIAGE JULY 14, 91. 

MIRANDA. 2/16/93. CAN'T HANDLE REGULAR 

MILK. BABY FORMULAS. EAR INFLAMMATION. 



D.M. 
GERMANY 



SON AND DAUGHTER BOTH CHRONICALLY ILL. 



K.M. 

DERRY. PA 15627 



BABY HAS SEVERE RESPIRATORY PROBLEMS 



(FROM RELATIVE OF VET) 
NEWTON, IL 62448 



BROTHER HAD A BABY THAT DIED AT 

15 MO AND A 2ND WITH ■'SEVERE PROBLEMS" 



A.M. 

CENTRAL TEXAS 



BABY WITH CLUBBED FEET, MISSING FINGERS. 
LEFT FACIAL PALSEY. EYE DEFECTS. 



G & R 

ABERDEEN PROVING GROUND 

MD 21005 



GREGORY. JR. OCT. 16. 1992. PHOCONELIA. 
SHORTNESS OF ARMS. MISSING ELBOW & BELOW. 
2 FINGERS. CAN'T GET UP ON HIS OWN. 



T & K 

MUSKEGON. MI 49442 



MISCARRIAGE. THEN HAD JANELLE, 10/27/93. 
GALL BLADDER TAKEN OUT. FULL OF STONES. 



GRANT, ALA 35747 



TIFFANY: DOB OCT. 3, 1992. 15 SYMPTOMS. 
CONSTANT RESPIRATORY/ ASTHMA CONDITION. 



R & T 

SHARON. WI 53586 



TAYLOR. 5/29/92. 3 OR MORE DEFORMITIES. 
SEVERE SLOWED GROWTH. NO WT GAIN 8 MO. 
TAYLOR HAD 27 SYMPTOMS, BUT IMPROVED 
WITH AMINO ACID NUTRITION. 



P 4 S 

MURRAY. UT 84107 



CHAD. 12/1/92. ICU FOR TWO WKS. ALLERGIC 
TO ADHESIVE TAPE. TOP COLON COLLAPSED. 
EAR INFECTIONS AND ANEMIA. DIARRHEA AND 
COLIC. 4 MO. OF BRONCHITIS. RESPIRATORY 
PROBLEMS. UNEXPLAINED RASHES. 



J & L 

LITTLE ROCK. ARK 72212 



JAMES. 1/28/92. IGA DEFICIENCY AND REFLUX. 
PERSISTENT COLDS DESPITE ANTIBIOTICS 



J & E 

HARVEY. LA 70058 



KATHERINE. 9/28/92. REPEATED EAR 
INFLAMMATION DESPITE ANTIBOTICS 



318 



J & A 

JERSEYVILLE, IL 62052 



BABY BOY WITH SEVERE RESPIRATORY 



P & A 

GREEN BAY. WI 54303 



ALEX. 6/28/93. MONTH LONG RASHES. 
EXCESSIVE CONSTIPATION. 



C.P. 

POSSIBLY HOUSTON, TX 



2 AS OF JUNE, 94. 
STARTED WALKING AT 23 MO. CROSSED EYES. 
SEVERE ALLERGIES. RASHES. LIVER PROB'S 
POOR MUSCLE TONE. DEMYLENATING CONDITION. 



C & D 

SAN DIEGO, CA 92105 



NEWBORN, JOSHUA, SICK 



J & T 

PURVIS, MS 39475 



RYAN, 5/31/92. VIRAL AND RESPIRATORY PROB. 
RYAN HAS MUSCLE WEAKNESS. TRIPS A LOT. 
RESPIRATORY PROB. SPIKING FEVERS. 



J & M 

LOUISVILLE, KY 40222 



MISCARRIAGE AROUND APR, 94. 



UKIAH, CALIF. 95482 



DAVID HAS MONTHLY VIRAL INFECTIONS. 



•COON RAPIDS, MN 55433 



3/12/93. PERSISTENT COLDS, 
EAR PROBLEMS. 



B.R. 

WEST GERMANY 



JAQUELINE, 9/23/92 HAS PERSISTENT COLDS 
DESPITE ANTIBIOTICS. EXCESSIVE DIARRHEA. 



STATIONED GI FAMILY IN EUROPE 
APO AE 09222 



BABY, SETHrDOB FEB. 23, 94. RPTS DIARRHEA 
AND VOMITING. DR'S CAN'T EXPLAIN VOMITING 
REACTIVE TO MILK AND BABY FORMULAS. 
FR. IS CHEMICALLY SENSITIVE. MOTHER ILL. 



A & D 

JACKSON, MS 39209 
MOTHER HAS 46 SYMPTOMS. 
FATHER ALSO ILL. 



AYLA, APP 2, HAS BABY DEFORMITIES 
IMMUNE SYS DOWN. FUSED FINGERS. PERSISTENT 
COUGH. SLOWED DEVELOPMENT, CONSTIPATION 
DIARRHEA. WATER POCKETS UNDER SKIN. 
ONE SIDE OF BABY'S BODY IS LARGER. 



T & T 

BENBROOK, TX 76126 



TONY, III. DIED 2 MO OF AGE. 
HUNTER, 3/12/94 IS NOW SICK. PERSISTENT 
COLD ABOUT 8 WKS. HUNTER HAS EXTRA TOES 
AND FINGERS. SNEEZING, ASTHMA AND 
RESPIRATORY PROBLEMS. HUNTER=13 SYMPTOMS. 



319 



B & S 

SHERIDAN, IN 46069 



SCOTT, HAS RESPIRATORY AND OTHER PROB. 
12/17/94. EARLY EAR INFLAMMATION. COLIC. 
TERRIBLE CONSTIPATION. DIARRHEA. 



R & S 

FLINT. MI 48506 



ROBERT, 6/16/92. 16 SYMPTOMS. PERSISTENT 
COOGH. COUGH MEDICINE. SPIKING FEVERS. 



B & N 
COLUMBIA. 



SC 29223-8.')15 



CHELSEA. 11/15/92. SQUEAKY HEART MURMUR. 
UNDERDEVELOPED ESOPHOGUS. ALSO HAD A 
MISCARRIAGE. 



G & M 

FAYETTEVILLE. NC. 28311 

MOTHER HAS 41 SYMPTOMS. 



GEORGE. 12/3/93 HAS UNEXPLAINED CHEST 
RASHES. PROB. WITH INITIAL BABY FORMULA. 
SEVERE BILATERAL CLEFT PALATE. PARTIAL 
HEARING LOSS. EAR INFLAMMATIONS. 



CEDAR RAPIDS. IOWA 52403 

MOTHER RECORDS 52 HEALTH SYMPTOMS 

HERSELF 



NICOLAS. 11/2/93. CLUBBED FEET. 19 SYMPTOMS 
DISLOCATED HIPS. AND ARTHOGRPOSIS 
MUTIPLEX CONGENTIA. REACTIVE TO CLNRS. 



E «c M 

BURKE, VA 22015 



HAYDEN, 11/4/92. BORN WITHOUT RT. EAR. 
DEAF, DEFORMED LEFT EAR. HAS OAV, 
OCULAR ARICULAR VERTEBRO. RT MANDIBLE IS 
SMALLER. SIX FINGERS ON RIGHT. ONE HAS 
BEEN SURGICALLY REMOVED. SCOLEOSIS. SOME 
VERTEBRAE HALVED. SOME FUSED. MOTHER 
INITIALLY HAD TWO MISCARRIAGES. NO 
APPARENT ALLERGIES. EAR CANAL ABNORMAL. 



A & P 

HATTIESBURG, MS 39401 



8/30/93 BABY. ARTIS WITH CHRONIC EAR 
PROBLEMS. EXCESSIVE VOMITING, DIARRHEA. 
CONSTIPATION. PERSISTENT COLDS DESPITE 
ANTIBIOTICS AND TROUBLESOME RASHES. 



FT. MEADE, MD 20755 

WAS, AND REMAINS. ACTIVE DUTY 



AMANDA DOB IS 11/6/93. 16 SYMPTOMS. 
SEVERAL SEVERE DEFORMITIES. PACYGYRA. 
CLEFT PALATE. CLEFT NOSE. LOW SET EAR 
LOBES, HYPOPLASTIC NAILS. HYPOPLASTIC 
NIPPLES. DIAPHRAGNMATIC HERNIA. 
HYDRONOTHROSIS. HIRSCHSPRUNGS DISEASE. 
ANTERIORLY DISPLACED ANUS. REFLUX. 
EXCEEDINGLY HIGH ALKALINE PHOSPHATE. 



CONROE, TX 77301 



BRITTNIE(SP?) AND NEWBORN IN DEC.RACHAEL 
BRITNIE ON MONITOR 8 MO. 



& R 

LAFAYETTE, INDIANA 47905 

FATHER IS SENSITIZED. 



2 MISCARRIAGES. 



320 



R & C 

ANNISTON. AL 36201 



SHEAN 6/22/92. REPEATED EAR INFECTIONS. 
INITIALLY, BREATHING WAS ABNORMAL. HAS 
WHEEZING AND ALLERGIES. 



D S 

LAFAYETTE, IN 47905 



TERESA HAS RASHES, BAD NIGHTSWEATS. 
SORES THAT DON'T HEAL. REACTIVE TO ADULT 
FOODS. 



FULTON, IL 61252 



2 MISCARRIAGES. 2 YR OLD DAUGHTER WITH 
UNEXPLAINED NIGHTSWEATS AND RASHES. 



BLAIRSVILLE, PA 15717 



MERISSA: 7/13/92. RESPIRATORY, COUGH, 
IMMUNODEFICIENCY. RASH SINCE BORN. 



K S 

FT. BRAGG, N.C. 28307 



MATHEW, 5/15/93. DIED MAR 94. 



M & J 

ELLSWORTH AFB, S.D. 57706 



AUSTIN. 12/21/93 DIED ON 5TH DAY. 
SYNDROMES OF MICROCEPHALY, MICROPHTHALMIA 
CATARACTS, AND JOINT CONTRACTURES. 



C i T 

MDRFREESBORO. TN 37129 



ALEX HAS CHRONIC ILLNESS. 



R & C 

FT. LEONARDWOOD, MO 65473 



CHELSEA. NOV 12 92. 24 SYMPTOMS. 
BABY HAS BRAIN DAMAGE. HARD TIME 
WALKING, SITTING UP, SHALLOWING, AND 
HOLDING OBJECTS. RASPY BREATHING 



ASHBOROUGH, NC 27203 



(2 MISCARRIAGES) 



WATERTOWN, S.D. 57201 
BOTH PARENTS ILL. 



TYLER, 2/21/92. RASHES ON CHEEKS. 
BORN W/RESPIRATORY DISTRESS- 5 WK PREMI 
CHRONIC EAR INFLAMMATION. ALLERGY AND 
ASTHMA PROBLEMS. 



J & D 

PHILADELPHIA. PA 19142 



2 YR OLD WITH ABNORMAL EAR INFECTIONS 
PERSISTENT COLDS 



LINDEN, NJ 07036 



MISCARRIAGE PLUS PROBLEMS WITH NEWBORN, 
SHANNON: MAR 13, 94. A VIRIS THAT'S A 
FORM OF HAND, FOOT, MOUTH DISEASE. 



D & A 

CLARA, MS 39324 



CHRONICALLY ILL BABY 



321 



B & L 

SPOONER. WI 54801 



BABY BORN DEAD W/NO KIDNEYS 
INTRAUTERINE GROWTH RETARDATION 
OLDER FAMILY CHILDREN ALSO AFFECTED 



W & R 

BARKER HEIGHTS, TX 76543 



BRANDON, 6/9/92. RESPIRATORY AND IS 
DEFICIENT IN HEMOGLOBINS (SP?). HAS 
PERSISTENT COLDS THAT SPREAD TO HEAD AND 
LUNGS. ORANGE WITH JAUNDICE WHEN BORN. 
REACTIVE TO PINESOL, SOFTSCRIB, AIR 
FRESHENERS. MUSCOUS MEMBRANES MESSED UP. 
TESTED POSI TO MOST OF 60 REG. ALLERGIES. 
MOTHER HAD MISCARRIAGE AFTER GULF. HAS 
HAD PNEMONIA 6 TIMES BY AUG. 94. 



J & T 

McKEESPORT, PA 15132 

FATHER IS ILL. 



PAIGE, 8/13/93. 
FOOT. 



HAS EXTRA TOE ON LEFT 



J & A 

CAPE CORAL, FL 

BOTH PARENTS ILL. 



ORIANA IS 2 1/2. ABNORMAL CHEST PAINS. 
RASHES WHEN AROUND FATHER. 



322 



CHRIST HOSPITAL 
P.O. iOX 939»2 
CHICAGO, It 60673 



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cALBUCK .ALEXANDER 



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'BaJOR CREDIT CARDS ACCEPTED. 



CALL (708)546-5079. 



. CM PLCASe PAT I MIS *M0<JNT i^>rM«nu Die lMlwu-.« w« MUmMt yev Owa. 
inpaM M your mavonc* wMI In Um Iron y9v " Thankyov. 

708381*878 08-03-94 06:aiPM P004 831 



323 



V 

E. R. ZUMWALT. JR. 

ADMIRAL. U S NAVY (RET.) 



August 4, 1994 



The Honorable John D. Rockefeller IV 
Chairman, U.S. Senate Veterans' 

Affairs Committee 
414 Russell Senate Office Building 
Washington, DC 20510 

Dear Mr. Chairman: 

I am grateful to the committee for its interest in the reproductive 
hazards of military personnel exposed to radiation. Agent Orange, 
and Desert Storm phenomena. Since I must be out of town on the day 
of the hearings, I submit the following statement: 

I am a veteran of three wars — World War II, Korea, and Vietnaun. I 
have seen an increase over the spectrum of those three wars in the 
dangers of exposure of our fighting men to hazards other than the 
shot and shell of battle. 

In my capacity as an unpaid special assistant to Secretary of 
Veterans Affairs, The Honorable Edward Derwinski, I conducted a 
study of the diseases resulting from the exposure of our Vietnam 
veterans in the Vietnam War. (As a commander in that War, I had 
authorized the use of Agent Orange to reduce the casualties to my 
naval men in the Brown Water Navy.) I attach a copy of the study 
which concludes that 28 diseases meet the criterion specified by 
law that it be "as likely as not" that they are caused by exposure 
to Agent Orange. Since that study was submitted, additional 
evidence has reinforced these conclusions and the Department of 
Veteran Affairs now authorizes compensation for nine of those 
diseases. In my judgement, the future reports of the National 
Academy of Sciences, as provided by law, will lead to the 
authorization of many of the remaining diseases identified in my 
study including the birth defects which my study identified as the 
result of Agent Orange exposure. 

Finally, the current EPA draft report (which should be finalized in 
September) on the effects of dioxin, a component of Agent Orange, 
provides further weight to the conclusions of my study concerning 
birth, developmental, and reproductive defects. 



324 



The Honorable John D. Rockefeller IV 
August 4, 1994 
Page Two 

I have had personal anecdotal evidence which reinforces my 
conviction. My son, Lieutenant JG Elmo Russell Zumwalt, III, a 
heavily Agent Orange exposed Vietnam veteran, died in 1988 after a 
five-year battle with non-Hodgkin ' s lymphoma and Hodgkin's 
lymphoma. His son, Elmo Russell Zumwalt, IV, has been diagnosed as 
having a sensory integration disfunction which makes learning 
extremely difficult. The anecdotal evidence which I encountered 
from among thousands of fellow Vietnam veterans further reenforces 
my conviction that birth, developmental, and reproductive defects 
result from exposure to Agent Orange. 

My second son. Lieutenant Colonel James G. Zumwalt, a veteran of 
both Vietnam and Desert Storm, experiences some symptoms of the 
Desert Storm Syndrome. I have encountered scores of other Desert 
Storm veterans who have similar problems. 

In the light of both my study experience and anecdotal evidence 
available to me, I strongly endorse the purpose of this committee. 

Sincerely, 




Sumwalt, Jr. 
Admizia/L, USN (Retired) 



1500 Wilson Boulevard, Suite 641 
Arlington, Virginia 22209 



(703) 527-5380 
Enclosure 



325 



REPORT TO THE SECRETARY OF THE DEPARTMENT OF VETERANS AFFAIRS 

ON THE ASSOCIATION BETWEEN ADVERSE HEALTH EFFECTS 

AND EXPOSURE TO AGENT ORANGE 



As Reported by Special Assistant 

Admiral E.R. Zumwalt, Jr. 

May 5, 1990 



326 



I. INTRODUCTION 

On October 6, 1989 I was appointed as special assistant to 
Secretary Derwinski of the Department of Veterans Affairs to 
assist the Secretary in determining whether it is at least as 
likely as not that there is a statistical association between 
exposure to Agent Orange and a specific adverse health effect. 

As special assistant, I was entrusted with evaluating the 
numerous data relevant to the statistical association between 
exposure to Agent Orange and the specific adverse health effects 
manifested by veterans who saw active duty in Vietnam. Such 
evaluations were made in accordance with the standards set forth 
in Public Law 98-542, the Veterans' Dioxin and Radiation Exposure 
Compensation Standards Act and 38 C.F.R. § 1.17, regulations of 
the Department of Veterans Affairs concerning the evaluation of 
studies relating to health effects of dioxin and radiation 
exposure. 

Consistent with my responsibilities as special assistant, I 
reviewed and evaluated the work of the Scientific Council of the 
Veterans ' Advisory Committee on Environmental Hazards and 
commissioned independent scientific experts to assist me in 
evaluating the validity of numerous human and animal studies on 
the effects of exposure to Agent Orange and/or exposure to 
herbicides containing 2,3,7,8 tetrachlorodibenzo-para-dioxin 
(TCDD or dioxin) . In addition, I reviewed and evaluated the 
protocol and standards employed by government sponsored studies 



327 



to assess such studies' credibility, fairness and consistency 
with generally accepted scientific practices. 

After reviewing the scientific literature related to the 
health effects of Vietnam Veterans exposed to Agent Orange as 
well as other studies concerning the health hazards of civilian 
exposure to dioxin contaminants, I conclude that there is 
adequate evidence for the Secretary to reasonably conclude that 
it is at least as likely as not that there is a relationship 
between exposure to Agent Orange and the following health 
problems: non-Hodgkin ' s lymphoma, chloracne and other skin 
disorders, lip cancer, bone cancer, soft tissue sarcoma, birth 
defects, skin cancer, porphyria cutanea tarda and other liver 
disorders, Hodgkin's disease, hematopoietic diseases, multiple 
myeloma, neurological defects, auto-immune diseases and 
disorders, leukemia, lung cancer, kidney cancer, malignant 
melanoma, pancreatic cancer, stomach cancer, colon cancer, 
nasal/pharyngeal/esophageal cancers, prostate cancer, testicular 
cancer, liver cancer, brain cancer, psychosocial effects and 
gastrointestinal diseases. 

I further conclude that the Veterans' Advisory Committee on 
Environmental Hazards has not acted with impartiality in its 
review and assessment of the scientific evidence related to the 
association of adverse health effects and exposure to Agent 
Orange. 

In addition to providing evidence in support of the 
conclusions stated above, this report provides the Secretary with 



328 



a review of the scientific, political and legal efforts that have 
occurred over the last decade to estedslish that Vietnam Veterans 
who have been exposed to Agent Orange are in fact entitled to 
compensation for various illnesses as service-related injuries. 

II. AGENT ORANGE USAGE IN VIETNAM 

Agent Orange was a 50:50 mixture of 2,4-D and 2,4,5-T. The 
latter component, 2,4,5-T, was found to contain the contaminant 
TCDD or 2,3,7,8-tetrachlorodiben2o-para-dioxin (i.e. dioxin) , 
which is regarded as one of the most toxic chemicals ]cnown to 
man.^ 

From 1962 to 1971 the United States military sprayed the 
herbicide Agent Orange to accomplish the following objectives: 1) 



See CDC Protocol for Epidemiologic Studies on the Health 
of Vietnam Veterans (November, 1983), p. 4 ( The CDC Protocol also 
contains a literature review as of 1983 of the health effects on 
animals and humans exposed to herbicides and dioxin, pp. 63-78. The 
literature review documents health problems such as chloracne, 
immunological suppression, neurological and psychological effects, 
reproductive problems such as birth defects, carcinogenic effects 
such as soft tissue sarcomas, lymphomas and thyroid tumors, and 
various gastrointestinal disorders) ; See also General Accounting 
Office, "Report by the Comptroller General: Health Effects of 
Exposure to Herbicide Orange in South Vietnam Should Be Resolved," 
GAO-CED-79-22 at 2 (April 6, 1979) [hereinafter GAO Report, 1979]. 
Dioxin is a family of chemicals (75 in all) that does not 
occur naturally, nor is it intentionally manufactured by any 
industry. The most toxic dioxin is called 2,3,7,8 - TCDD. Dioxins 
are produced as byproducts of the manufacture of some herbicides 
(for example, 2,4,5-T), wood preservatives made from 
trichlorophenals, and some germicides. Dioxins are also produced 
by the manufacture of pulp and paper, by the combustion of wood in 
the presence of chlorine, by fires involving chlorinated benzenes 
and biphenyls (e.g. PCBs) , by the exhaust of automobiles burning 
leaded fuel, and by municipal solid waste incinerators. 



329 



defoliate jungle terrain to improve observation and prevent enemy 
ambush; 2) destroy food crops; and 3) clear vegetation around 
military installations, landing zones, fire base camps, and 
trails.^ 

Unlike civilian applications of the components contained in 
Agent Orange which are diluted in oil and water, Agent Orange was 
sprayed undiluted in Vietnam. Military applications were sprayed 
at the rate of approximately 3 gallons per acre and contained 
approximately 12 pounds of 2,4-D and 13.8 pounds of 2,4,5-T.' 

Although the military dispensed Agent Orange in 
concentrations 6 to 25 times the manufacturer's suggested rate, 
"at that time the Department of Defense (DOD) did not consider 
herbicide orange toxic or dangerous to humans and took few 
precautions to prevent exposure to it."* Yet, evidence readily 
suggests that at the time of its use experts knew that Agent 
Orange was harmful to military personnel.* 



See Bruce Myers, "Soldier of Orange: The Administrative, 
Diplomatic, Legislative and Litigatory Impact' of Herbicide Agent 
Orange in South Vietnam," 8 B. C. Env't. Aff. L. Rev. 159, 162 
(1979) . 



Env't Aff. L. Rev, at 162. In contrast, civilian applications of 
2,4,5-T varied from 1 to 4 pounds per acre. 

* General Accounting Office, "Ground Troops in South Vietnam 
Were in Areas Sprayed with Herbicide Orange," FPCD 80-23, p.l 
(November 16, 1979) . 

' Letter from Dr. James R. Clary to Senator Tom Daschle 
(September 9, 1988) . Dr. Clary is a former government scientist 
with the Chemical Weapons Branch, BW/CW Division, Air Force 
Armament Development Laboratory, Eglin AFB, Florida. Dr. Clary was 
instrumental in designing the specifications for the A/A 45y-l 
spray tank (ADO 42) and was also the scientist who prepared the 



330 



The bulk of Agent Orange herbicides used in Vietnam were 
reportedly sprayed from "Operation Ranch Hand" fixed wing 
aircraft. Smaller quantities were applied from helicopters, 
trucks, riverboats, and by hand. Although voluminous records of 
Ranch Hand missions are contained in computer records, otherwise 
known as the HERBS and Service HERBs tapes, a significant, if 
not major source of exposure for ground forces was from non- 
recorded, non Ranch Hand operations.^ 

Widespread use of Agent Orange coincided with the massive 
buildup of U.S. military personnel in Vietnam, reaching a peak in 



final report on Ranch Hand: Herbicide Operations in SEA, July 1979. 
According to Dr. Clary: 

When we (military scientists) initiated the herbicide program 
in the 1960's, we were aware of the potential for damage due 
to dioxin contamination in the herbicide. We were even aware 
that the 'military* formulation had a higher dioxin 
concentration than the 'civilian' version due to the lower 
cost and speed of manufacture. However, because the material 
was to be used on the 'enemy', none of us were overly 
concerned. We never considered a scenario in which our own 
personnel would become contaminated with the herbicide. And, 
if we had, we would have expected our own government to give 
assistance to veterans so contaminated. 

See also notes 13, 73-75 and accompanying text infra for 
additional information of the manufacturer's awareness of the 
toxicity of Agent Orange. 

* Combat units, such as the "Brown Water Navy," frequently 
conducted "unofficial" sprayings of Agent Orange obtained from out 
of channel, and thus unrecorded sources. Additionally, as 
Commander, U.S. Naval Forces, Vietnam, I was aware that Agent 
Orange issued to Allied forces was frequently used on unrecorded 
missions. 



331 



1969 and eventually stopping in 197 l/ Thus, according to an 
official of the then Veterans Administration, it was 
"theoretically possible that about 4.2 million American soldiers 
could have made transient or significant contact with the 
herbicides because of [the Ranch Hand Operation]." ' 

A. REASONS FOR PHASE OUT 

Beginning as early as 1968, scientists, health officials, 
politicians and the military itself began to express concerns 
about the potential toxicity of Agent Orange and its contaminant 
dioxin to humans. For instance, in February 1969 The Bionetics 
Research Council Committee ("BRC") in a report commissioned by 
the United States Department of Agriculture found that 2,4,5-T 
showed a "significant potential to increase birth defects." ' 
Within four months after the BRC report, Vietnamese newspapers 
began reporting significant increases in human birth defects 



accompanying text infra for a discussion of the correlation between 
the spraying of Agent Orange and the hospitalization of Vietnam 
soldiers for disease and non-battle related injuries. 

' House Comm. on Veteran's Affairs, 95th Cong., 2d Sess., 
Herbicide "Aaent Oranae" . Hearings before the Subcommittee on 
Medical Facilities and Benefits . (Oct. 11, 1978) (Statement of Ma j . 
Gen. Garth Dettinger USAF, Deputy Surgeon General USAF at 12) . 

' Myers at 166. 

^° I^. While birth defects did significantly increase in 
Saigon, critics contend that Saigon was not an area where the 
preponderance of defoliation missions were flown and argue that 
such increases were due primarily to the influx of U.S. medical 
personnel who kept better records of birth defects. Subsequent 



332 



By October, 1969, the National Institute of Health confirmed 
that 2,4,5-T could cause malformations and stillbirths in mice, 
thereby prompting the Department of Defense to announce a partial 
curtailment of its Agent Orange spraying," 

By April 15, 1970, the public outcry and mounting scientific 
evidence caused the Surgeon General of the United States to issue 
a warning that the use of 2,4,5-T might be hazardous to "our 
health" . " 

On the same day, the Secretaries of Agriculture, Health 
Education and Welfare, and the Interior, stirred by the 
publication of studies that indicated 2,4,5-T was a teratogen 
(i.e. caused birth defects), jointly announced the suspension of 
its use around lakes, ponds, ditch banks, recreation areas and 



studies in Vietnam confirm the incidence of increased birth defects 
among civilian populations exposed to Agent Orange. See e.g. 
Phuong, et. al. "An Estimate of Reproductive Abnormalities in Women 
Inhabiting Herbicide Sprayed and Non-herbicide Sprayed Areas in the 
South of Vietnam, 152-1981 18 Chemosphere 843-846 (1989) 
(significant statistical difference between hydatidiform mole and 
congenital malformations between populations potentially exposed 
and not exposed to TCDD) ; Phuong, et. al., "An Estimate of 
Differences Among Women Giving Birth to Deformed Babies and Among 
Those with Hydatidiform Mole Seen at the OB-GYN Hospital of Ho Chi 
Minh City in the South of Vietnam," 18 Chemosphere 801-803 (1989) 
(statistically significant connection between frequency of the 
occurrence of congenital abnormalities and of hydatidiform moles 
and a history of phenoxyherbicide exposure); Huong, et. al., "An 
Estimate of the Incidence of birth Defects, Hydatidiform Mole and 
Fetal Death in Utero Between 1952 and 1985 at the OB-GYN Hospital 
of Ho Chi Minh City, Republic of Vietnam," 18 Chemosphere 805-810 
(1989) (sharp increase in the rate of fetal death in utero, 
hydatidiform mole (with or without choriocarcinoma) and congenital 
malformations from the pre 1965-1975 period, suggesting possible 
association to phenoxyherbicide exposure) . 

" Myers at 167 



333 



The Department 

of Defense simultaneously announced its suspension of all uses of 
Agent Orange." 

B. HEALTH STUDIES 

As Agent Orange concerns grew, numerous independent studies 
were conducted between 1974 and 1983 to determine if a link 
exists between certain cancerous diseases, such as non-Hodgkin ' s 
lymphoma and soft-tissue sarcomas, and exposure to the chemical 
components found in Agent Orange. These studies suggested just 
such a link. 

In 1974, for example. Dr. Lennart Hardell began a study 
which eventually demonstrated a statistically significant 
correlation between exposure to pesticides containing dioxin and 



of 2,4,5-T and 2,4-D, denied this teratogenicity, Dow's own tests 
confirmed that when dioxin was present in quantities exceeding 
production specifications, birth defects did occur. See J. 
McCullough, Herbicides; Environmental He alth Effects; Vietnam and 

thS Geneva Prqtpg*?! ; peve;opmept;s Pmrtpq 1222, 13 (1970) 

(Congressional Research Report No. UG 447, 70-303SP) . Pressure from 
industry subsequently led to some relaxation of the limits placed 
on the 2,4,5-T and 2,4-D. The only current uses for these chemicals 
in the United States are on rice, pastures, rangelands and rights 
of way. 

" I^. at 167. See also ppw Ch?Tnj,ca; v. RycHglsnayg, 477 F. 
2d 1317, 1319 (8th Cir. 1973) (secretaries announcement quoted in 
the opinion) . 

" Hardell, L. and Sandstrom, A. "Case-control Study: Soft 
Tissue Sarcomas and Exposure to Phenoxyacetic Acids or 
Chlorophenols," 39 Brit. J. Cancer . 711-717 (1979). See also note 
89 infra for the confirming results of follow-up studies by Hardell 
and others. 



334 



In 1974, Axelson and Sundell reported a two-fold increase of 
cancer in a cohort study of Swedish railway workers exposed to a 
variety of herbicides containing dioxin contaminants.^' 

By 1976, the Occupational Safety and Health Administration, 
esteiblished rigorous exposure criteria for workers working with 
2,4,5-tJ' 

In 1977 the International Agency for Research on Cancer 
(lARC) , while cautioning that the overall data was inconclusive, 
reported numerous anomalies and increased mortality rates in 
animals and humans exposed to 2,4-D or 2,4,5-T.^' 



Axelson emd Sundell, "Herbicide Exposure, Mortality and 
Tumor Incidence: An Epidemiological Investigation on Swedish 
Railroad Workers," 11 Work Env't. Health 21-28 (1974). 

" U.S. Occupational Safety and Health Administration (1976), 
Air Contaminants; U.S. Code, Federal Register 29, Part 1910.93 at 
p. 27. 

^* with regard to 2,4-D, the lARC found the following 
anomalies: elevated levels of cancer in rats; acute and short-tet^ 
oral toxicity in mice, reLbbits, guinea pigs and rats — death, 
stiffness in the extremities, incoordination, stupor, myotonia, and 
other physical aJanormalities; in monkeys, injections caused nausea, 
vomiting, lethargy, muscular incoordination and head droop, fatty 
degeneration of the liver, spleen, kidneys and heart; foetal 
anomaly increases in some species; post-birth death rates increased 
in some species; higher mortality rates and morphological 
alterations in pheasant embryos and their chicks when spraying took 
place under simulated field conditions; higher mortality rates in 
rat pups in a 3 generation exposure; gene mutation after exposure 
to high concentrations; chromosomal aberrations when cultured human 
lymphocytes were exposed; increased frequency of aberrant 
metaphases (2 to 4 times) in mice exposed to toxic concentrations. 

In humans the lARC found that: a 23 year old farming student, 
a suicide, had 6 grams of 2,4-D in his body, acute congestion of 
all organs, severe degeneration of ganglion cells in the central 
nervous system; 3 cases of peripheral neuropathy in humans sprayed 
with 2,4-D with initial symptoms of nausea, vomiting, diarrhea, 
swelling and aching of feet and legs with latency, in individual 
cases, paresthesia in the extremities, pain in the legs, numbness 
and aching of fingers and toes, swelling in hand joints, flaccid 

10 



335 



In 1978, the Environnental Protection Agency issued an 
eoergency suspension of the spraying of 2,4,5-T in national 
forests after finding "a statistically significant increase in 
the frequency of miscarriages" among women living near forests 
sprayed with 2,4,5-T.^' 

In 1980, another provocative mortality study of workers 



parapheresis; similar case reports in agriculture workers sprayed 
by 2,4-D; workers associated with 2,4-0 developed symptoms of 
somnolence, anorexia, gastralgia, increased salivation, a sweet 
taste in the mouth, a sensation of drunkenness, heaviness of the 
legs and hyperacusea, rapid fatigue, headache, loss of appetite, 
pains in the region of liver and stomach, weakness, vertigo, 
hypotension, - bradycardia, dyspeptic symptoms, gastritis, liver 
disfunction, changes in metabolic processes. 

With regard to 2,4,5-T's effect on animals the lARC found: it 
can increase the frequency of cleft palates in some strains of 
mice; fetal growth retardation may also be observed; cystic 
kidneys were observed in two strains of mice; in purest available 
form, it induced some fetal effects and skeletal anomalies in rats 
as well as behavioral aJ3normalities, changes in thyroid activity 
and brain serotonin levels in the progeny; increases in 
intrauterine deaths and in malformations in rats; fetal death and 
teratogenic effects in Syrian golden hauasters; chromosomal 
abnormalities. 

The lARC reported in 1977 with respect to 2,4,5-T's effects 
on humans that: workers exposed at a factory in the USSR had skin 
lesions, acne, liver impairment, and neurasthenic syndrome; similar 
findings were reported by Jerasneh, et al (1973, 1974) in a factory 
in Czechoslovakia which in 1965-68 produced 76 cases of chloracne, 
2 deaths from bronchogenic cancers. Some workers had porphyria 
cutanea tarda, urophry imuria , aibnormal liver tests, severe 
neurasthenia, depression syndrome, peripheral neuropathy; in a 1975 
accident in West Virginia, 228 people were affected. Symptoms 
included chloracne, melanosis, muscular aches and pains, fatigue, 
nervousness, intolerance to cold; 4 workers of 50 affected in a 
similar accident in the Netherlands in 1963 died within 2 years 
and at least 10 still had skin complaints 13 years later. 

^' June 1979 Congressi onal Hearings before House Commerce 
Committee. Subcommittee on Oversig ht and Investigations, quoted in 
"Hximan Disease Linked to Dioxin: Congress Calls for 2,4,5-T Ban 
After Dramatic Herbicide Hearings", 28 Bioscience 454 (August 
1979). This study, otherwise known as the Alsea Study, has been 
cited as showing the first correlation between 2,4,5-T (and 
presumably its TCDD contaminant) and teratogenic effects in humans. 

11 



336 



involved in an accident at an industrial plant which manufactured 
dioxin compounds suggested that exposure to these compounds 
resulted in excessive deaths from neoplasms of the lymphatic and 
hematopoietic tissues.^ 

On September 22, 1980, the U.S. Interagency Work Group to 
Study the Long-term Health Effects of Phenoxy Herbicides and 
Contaminants concluded "that despite the studies' limitations, 
they do show a correlation between exposure to phenoxy acid 
herbicides and an increased risk of developing soft-tissue tumors 
or malignant lymphomas."^' 

To be sure, there remain skeptics who insist that the 
studies failed in one respect or another to establish a 
scientifically acceptable correlation.^ Yet, it can fairly be 
said that the general attitude both within and outside the 
scientific community was, and continues to be increasing concern 
over the mounting evidence of a connection between certain cancer 



^ Zack and Suskind, "The Mortality Experience of Workers 
Exposed to TCDD in a Trichlorophenol Process Accident," 22 Journal 
<?f M?^i<?ine, 11-14 (1980). 



Health Effects of Phenoxy Herbicides and Contaminants (September 
22, 1980) (executive summary). 



Carcinogenicity of 2,4-D" (January 1990) (This report, sponsored 
by the National Association of Wheat Growers Foundation and a grant 
from the Industry Task Force II on 2,4-D Research Data, an 
association of manufacturers and commercial formulators of 2,4-D, 
concluded that the toxicological data on 2,4-D does not provide a 
strong basis for predicting that 2,4-D is carcinogenic to humans. 
Nevertheless, the panel reviewing the evidence did conclude that 
"evidence indicates that it is possible that exposure to 2,4-D can 
cause cancer in humans."). 

12 



337 



illnesses and exposure to dioxins'. 



III. VETERANS' DIOXIN AND RADIATION EXPOSURE COMPENSATION 
STANDARDS ACT OF 1984 



With the increasing volume of scientific literature giving 
credenc? to the belief of many Vietnam Veterans that exposure to 
Agent Orange during their military service was related to their 
contraction of several debilitating diseases — particularly non- 
Hodgkin's lymphoma, soft tissue sarcoma ("STS") (malignant tumors 
that form in muscle fat, or fibrous connective tissue) and 
porphyria cutanea tarda ("PCT") (deficiencies in liver enzymes) — 
Vietnam Veterans rightfully sought disability compensation from 
the Veterans Administration ("VA") . 

The VA determined, however, that the vast majority of 
claimants were not entitled to compensation since they did not 
have service connected illnesses.^ As a consequence. Congress 
attempted to alter dramatically the process governing Agent 
Orange disability claims through passage of the Veterans' Dioxin 
and Radiation Exposure Compensation Standards Act of 1984 



" By October 1, 1983, 9170 veterans filed claims for 
disabilities that they alleged were caused by exposure to Agent 
Orange. The VA denied compensation to 7709 claimants on the grounds 
that the claimed diseases were not service connected. Only one 
disease was deemed associated with service related exposure to 
Agent Orange, a skin condition known as chloracne. See House 
Report No. 98-592, reprinted in U.S. Code Cong. & Adm. News, 98th 
Cong. 2d Sess.,1984, at 4452. See also Nehmer v. U-S. Veterans 
ftdmip3,stC?ti9n, 712 F.Supp. 1404, 1407 (1989). 

13 



338 



(hereinafter the "Dioxin Standards Act") .^* To ensure that the 
VA provided disability compensation to veterans exposed to 
herbicides containing dioxin while serving in Vietnam,^ Congress 
authorized the VA to conduct rulemaking to determine those 
diseases that were entitled to compensation as a result of a 
service-related exposure to Agent Orange.^ 

In promulgating such rules, the Dioxin Standards Act 
required the VA to appoint a Veterans' Advisory Committee on 
Environmental Hazards (the "Advisory Committee") — composed of 
experts in dioxin, experts in epidemiology, and interested 
members of the public — to review the scientific literature on 
dioxin and submit periodic recommendations and evaluations to the 
Administrator of the VA.^ Such experts were directed to 
evaluate the scientific evidence pursuant to regulations 
promulgated by the VA, and thereafter to submit recommendations 



Standards Act, Pub. L. 98-542, Oct. 24, 1984, 98 Stat. 2727 
(hereinafter the Dioxin Standards Act) . In passing the Act Congress 
found that Vietnam Veterans were "deeply concerned about possible 
long term health effects of exposure to herbicides containing 
dioxin," (Section 2 (1)), particularly since "[t]here is scientific 
and medical uncertainty regarding such long-term adverse health 
effects." (Section 2 (2)). In responding to this imcertainty. 
Congress mandated that "thorough epidemiological studies of the 
health effects experienced by veterans in connection with exposure 
...to herbicides containing dioxin" be conducted, (Section 2(4)), 
especially in light of the fact that "[t]here is some evidence that 
chloracne, porphyria cutanea tarda, and soft tissue sarcoma are 
associated with exposure to certain levels of dioxin as found in 
some herbicides." (Section 2 (5)). 

^ Id^ at Section 3. 

^ Id. at Section 5. 



and evaluations to the Administrator of the VA on whether "sound 

scientific or medical evidence" indicated a connection to 

exposure to Agent Orange and the manifestation of various 

diseases.^' 

In recognition of the uncertain state of scientific evidence 

and the inability to make an absolute causal connection between 

exposure to herbicides containing dioxin and affliction with 

various rare cancer diseases,^ Congress mandated that the VA 

Administrator resolve any doubt in favor of the veteran seeking 

compensation. As stated in the Dioxin Standards Act: 

It has always been the policy of the Veterans Administration 
and is the policy of the United States, with respect to 
individual claims for service connection of diseases and 
disabilities, that when, after consideration of all the 
evidence and material of record, there is an approximate 
balance of positive and negative evidence regarding the 
merits of an issue material to the determination of a claim, 
the benefit of the doxibt in resolving each such issue shall 
be given to the claimant.'" 

A. NEHMER V. U.S. VETERANS ADMINISTRATION 

Despite Congressional intent to give the veteran the benefit 
of the doubt, and in direct opposition to the stated purpose of 



"Id. at Section 5. 

^ S£g Nehmer v. U.S. Veterans Admin.. 712 F. Supp. 1404, 
1418 (N.D. Cal. (1989) wherein the court found after reviewing the 
legislative history of the Act "that Congress intended service 
connection to be granted on the basis of 'increased risk of 
incidence', or a 'significant correlation' between dioxin and 
various diseases," rather than on the basis of a causal 
relationship. 



30 



See Dioxin Standards Act at Section 2 (13) 
15 



340 



the Dioxin Standards Act to provide disability conpensation to 
Vietnam Veterans suffering with cancer who were exposed to Agent. 
Orange, the VA continued to deny compensation improperly to over 
31,000 veterans with just such claims. In fact, in promulgating 
the rules specified by Dioxin Standards Act, the VA not only 
confounded the intent of the Congress, but directly contradicted 
its own established practice of granting compensable service- 
connection status for diseases on the lesser showing of a 
statistical association, promulgating instead the more stringent 
requirement that compensation depends on esteiblishing a cause and 
effect relationship.'^ 

Mounting a challenge to the regulations. Veterans groups 
prosecuted a successful legal action which found that the VA had 
"both imposed an impennissibly demanding test for granting 
service connection for various diseases and refused to give the 



'^ See e.g. 38 C.F.R. § 3.310(b) (compensation granted for 
cardiovascular diseases incurred by veterans who suffered 
amputations of legs or feet); Nehmer at 1418. 

The significance of the distinction between a statistical 
association and a cause and effect relationship is in the burden 
of proof that the veteran must satisfy in order to be granted 
benefits. A statistical association "means that the observed 
coincidence in variations between exposure to the toxic substance 
and the adverse health effects is unlikely to be a chance 
occurrence or happenstance," whereas the cause and effect 
relationship "describes a much stronger relajtionship between 
exposure to a particular toxic substance and the development of a 
particular disease than 'statistically significant association' 
does." Nehmer . 712 F.Supp. at 1416. 

Thus, the regulation promulgated by the VA established an 
overly burdensome standard by incorporating the causal relationship 
test within the text of the regulation itself. 38 C.F.R. § 3.311(d) 
(••[s]ound scientific and medical evidence does not establish a 
cause and effect relationship between dioxin exposure" and any 
diseases except some cases of chloracne) (emphasis added) . 

16 



341 



veterans the benefit of the doubt in meeting the demanding 
standard." Nehmer v. U.S. Veterans Administration. 712 F. Supp. 
1404, 1423 (1989) (emphasis in original). As a result, the court 
invalidated the VA's Dioxin regulation which denied service 
connection for all diseases other than chloracne; ordered the VA 
to amend its rules; and further ordered that the Advisory 
Committee reassess its recommendations in light of the court's 
order." 

Thus, on October 2, 1989, the VA amended 38 C.F.R. Part 1, 
which among other things set forth various factors for the 
Secretary and the Advisory Committee to consider in determining 
whether it is "at least as likely as not" that a scientific study 
shows a "significant statistical association" between a 
particular exposure to herbicides containing dioxin and a 



" 38 C.F.R. § 1.17 (b) & (d). 38 C.F.R. § 1,17 states: 

(a) From time to time, the Secretary shall publish evaluations 
of scientific or medical studies relating to the adverse health 
effects of exposure to a herbicide containing 2,3,7,8 
tetrachlorodibenzo-p-dioxin (dioxin) and/or exposure to ionizing 
radiation in the "Notices" section of the Federal Register . 

(b) Factors to be considered in evaluating scientific studies 
include: 

(1) Whether the study's findings are statistically significant 
and replicable. 

(2) Whether the study and its findings have withstood peer 
review. 

(3) Whether the study methodology has been sufficiently 
described to permit replication of the study. 

(4) Whether the study's findings are applicable to the veteran 
population of interest. 

(5) The views of the appropriate panel of the Scientific Council 
of the Veteran' Advisory Committee on Environmental Hazards. 

(c) When the Secretary determines, based on the evaluation of 

17 



342 



regulation permits the Secretary to disregard the findings of the 
Advisory Committee, as well as the standards set forth at 38 



scientific or medical studies and after receiving the advice of the 
Veteran's Advisory Committee on Environmental Hazards and applying 
the reasonable doubt doctrine as set forth in paragraph (d) (1) of 
this section, that a significant statistical association exists 
between any disease and exposure to a herbicide containing dioxin 
or exposure to ionizing radiation, §§ 3.311a or 3.311b of this 
title, as appropriate, shall be eunended to provide guidelines for 
the establishment of service connection. 

(d) (1) For purposes of paragraph (c) of this section a 
"significant statistical association" shall be deemed to exist when 
the relative weights of valid positive and negative studies permit 
the conclusion that it is at least as likely as not that the 
purported relationship between a particular type of exposure and 
a specific adverse health effect exists. 

(2) For purposes of this paragraph a valid study is one which: 
(i) Had adequately described the study design and methods of 

data collection, verification and analysis; 

(ii) Is reasonzQaly free of biases, such as selection, 
observation and participation biases; however, if biases exist, the 
investigator has acknowledged them and so stated the study's 
conclusions that the biases do not intrude upon those conclusions; 
and 

(iii) Has satisfactorily accounted for known confounding 
factors. 

(3) For purposes of this paragraph a valid positive study is one 
which satisfies the criteria in paragraph (d) (2) of this section 
and whose findings are statistically significant at a probability 
level of .05 or less with proper accounting for multiple 
comparisons and subgroups analyses. 

(4) For purposes of this paragraph a valid negative study is one 
which satisfies the criteria in paragraph (d) (2) of this section 
and has sufficient statistical power to detect an association 
between a particular type of exposure and a specific adverse health 
effect if such an association were to exist. 

(e) For purposes of assessing the relative weights of valid 
positive and negative studies, other studies affecting 
epidemiological assessments including case series, correlational 
studies and studies with insufficient statistical power as well as 
key mechanistic and animal studies which are found to have 
particular relevance to an effect on human organ systems may also 
be considered. 

(f) Notwithstanding the provisions of paragraph (d) of this 
section, a "significant statistical association" may be deemed to 
exist between a particular exposure and a specific disease if, in 
the Secretary's judgment, scientific and medical evidence on the 
whole supports such a decision. 

18 



343 



C.F.R. § 1.17 (d) and determine in his own iudcment that the 
scientific and medical evidence supports the existence of a 
"significant statistical association" between a particular 
exposure and a specific disease. 38 C.F.R. S 1.17 (f) . 

The Secretary recently exercised his discretionary authority 
under this rule when he found a significant statistical 
association between exposure to Agent Orange and non-Hodgkin • s 
lymphoma, notwithstanding the failure of his own Advisory 
Committee to recommend such action in the face of overwhelming 
scientific data.'* 



B. THE WORK OF THE VETERANS' ADVISORY COMMITTEE ON 
ENVIRONMENTAL HAZARDS 



To assess the validity and competency of the work of the 
Advisory Committee, I asked several impartial scientists to 



of which were deemed to be valid positive in demonstrating the link 
between exposure to herbicides containing dioxin and non-Hodgkin ' s 
lymphoma, the Advisory Committee still concluded that: 

The Committee does not find the evidence sufficient at the 
present time to conclude that there is a significant 
statistical association between exposure to phenoxy acid 
herbicides and non-Hodgkin • s lymphoma. However, the Committee 
cannot rule out such an association. 

The Secretary should be interested to note that a new 
mortality study positively confirms that farmers exposed to 
herbicides containing 2,4-D have an increased risk of developing 
non-Hodgkin ' s lymphoma. See Blair, "Herbicides and Non-Hodgkin ' s 
Lymphoma: New Evidence From a Study of Saskatchewan Farmers," 82 
Journal of the National Cancer Institute 575-582 (1990). 



344 



review the Advisory Committee transcripts. Without exception, 
the experts who reviewed the work of the Advisory Committee 
disagreed with its findings and further questioned the validity 
of the Advisory Committee's review of studies on non-Hodgkin • s 
lymphomas . 

For instance, a distinguished group at the Fred Hutchinson 
Cancer Research Institute in Seattle, Washington, upon reviewing 
the Advisory Committee transcripts, concluded "that it is at 
least as likely as not that there is a significant association 
(as defined by the Secretary of Veterans Affairs) between 
[exposure to phenoxy acid herbicides and non-Hodgkin ' s 
lymphoma . ] " " This same group f uirther asserts that the 
Committee's work was "not sensible" and "rather unsatisfactory" 
in its review and classification of the various studies it 
reviewed. Additionally, these scientists regarded Dr. Lathrop's 
views as "less than objective" and felt that the possibility 
exists that "his extreme views (e.g., in respect to the role of 
dose-response testing) may have unduly affected the Committee's 
work." Finally, the Hutchinson scientists argue that the issue 
of chemical-specific effects, in which animal studies have been 
sufficient to demonstrate the carcinogenicity of dioxin, is an 
important factor "not well considered by the Committee." 
(emphasis in original) 

A second reviewer of the Committee's work. Dr. Robert 



Letter to Admiral Zumwalt from Dr. Robert W. Day, Director 
of the Fred Hutchinson Cancer Research Center of Seattle, 
Washington (Feb. 20, 1990). 

20 



345 



Hartzaan (considered one of the U.S. Navy's top medical 

researchers) , effectively confirms the views of the Hutchinson 

group. Dr. Hartzman states that "the preponderance of evidence 

from the papers reviewed [by the Advisory Committee] weighs 

heavily in favor of an effect of Agent Orange on increased risk 

for non-Hodgkin • s lymphoma."" Dr. Hartzman also attests that: 

an inadequate process is being used to evaluate scientific 
publications for use in public policy. The process uses 
scientific words like 'significant at the 5% level' and a 
committee of scientists to produce a decision about a series 
of publications. But in reality, the Committee was so tied 
by the process, that a decision which should have been based 
on scientific data was reduced to vague impressions — 
Actually, if the reading of the rules of valid negative 
found in the transcript is correct ('a valid negative must 
be significant at the p=.05 level' that is statistically 
significant on the negative side) none of the papers 
reviewed are valid negatives. 

A third reviewing teaun, Dr. Jeanne Hager Stellman, PhD 

(Physical Chemistry) and Steven D. Stellman, PhD (Physical 

Chemistry) , also echo the sentiments expressed by the Hutchinson 

Group and Dr. Hartzman on the validity of the Committee's 

proceedings and conclusions. In fact, the Stellmans' detailed 

annotated bibliography and assessment of numerous cancer studies 

relevant to herbicide exposure presents a stunning indictment of 

the Advisory Committee's scientific interpretation and policy 

judgments regarding the link between Agent Orange and Vietnam 



" Letter to Admiral Zumwalt from Dr. R.J. Hartzman Capt. MC 
USN (March 7, 1990) . 

" Id. at p. 3. 

21 



346 



Veterans . 

A fourth reviewer, a distinguished scientist intimately 

associated with government sponsored studies on the effects of 

exposure to Agent Orange, states the same conclusions reached by 

the other reviewers: 

The work of the Veterans' Advisory Committee on 
Environmental Hazards, as documented in their November 2, 
1989 transcript, has little or no scientific merit, and 
should not serve as a basis for compensation or regulatory 
decisions of any sort... 

My analysis of the NHL articles reviewed by the committee 
reveals striking patterns which indicate to me that it is 
much more likely than not that a statistical association 
exists between NHL and herbicide exposure." 

As these various reviewers suggest, the Advisory Committee's 
conclusions on the relationship between exposure to Agent Orange 
and non-Hodgkin ' s lymphoma were woefully understated in light of 
the clear evidence demonstrating a significant statistical 
association between NHL and exposure to phenoxy acid herbicides 
such as Agent Orange. 

Perhaps more significant than the Committee's failure to 
make such obvious findings is the distressing conclusion of the 
independent reviewers that the Committee's process is so flawed 



Commentaries Relevant to the Science Interpretation and Policy: 
Agent Orange and Vietnam Veterans," (March 1, 1990). See also note 
51 and accompanying text infra for additional discussion of the 
Stellmans' work. 



available for the Secretary's personal inspection and review. In 
another paper, this same source stated: "I estimate that the 
[Vietnam] Veterans are experiencing a 40% to 50% increase in 
sarcomas and non-Hodgkin ' s lymphoma rates." 

22 



347 



as to be useless to the Secretary in Baking any determination on 
the effects of Agent Orange. From a mere reading of Committee 
transcripts, these reviewers detected overt bias in the 
Committee's evaluation of certain studies. In fact, some members 
of the Advisory Committee and other VA officials have, even 
before reviewing the evidence, publicly denied the existence of a 
correlation between exposure to dioxins and adverse health 
effects.*" This blatant lack of impartiality lends credence to 
the suspicion that certain individuals may have been unduly 
influenced in their evaluation of various studies. Furthermore, 
such bias among Advisory Committee members suggests that the 
Secretary should, in accordance with the Dioxin Standards Act, 
appoint new personnel to the Advisory Committee. 

III. THE CDC STUDIES 

Were the faulty conclusions, flawed methodology and 
noticeable bias of the Advisory Committee an isolated problem, 
correcting the misdirection would be more manageable. But, 
experience with other governmental agencies responsible for 
specifically analyzing and studying the effects of exposure to 



*" For instance, Dr. Lawrence B. Hobson (Director, Office of 
Environmental Medicine, Veterans Health Services and Research 
Administration) , claims that TCDD "presents no threat from the 
exposures experienced by the veterans and the public at large," and 
virtually accuses scientists who find that such health effects do 
exist to be nothing more than witch doctors. See Hobson, "Dioxin 
and Witchcraft" presented at the 5th International Symposium on 
Chlorinated Dioxins and Related Compounds (September 1985) . 



348 



Agent Orange strongly hints at a discernible pattern, if not 
outright governmental collaboration, to deny compensation to 
Vietnam Veterans for disabilities associated with exposure to 
dioxin. 

A case in point is the Centers for Disease Control ("CDC"). 
As concerns grew following the first studies of human exposure to 
Agent Orange, Congress commissioned a large scale epidemiological 
study to determine the potential health effects for Vietnam 
Veterans exposed to Agent Orange. Initially, this study was to 
be conducted by the VA itself. When evidence surfaced, however, 
of the VA's footdragging in commencing the study (and initial 
disavowal of any potential harm from exposure to Agent Orange) , 
Congress transferred the responsibility for the study to the CDC 
in 1983.*' 

Unfortunately, as hearings before the Human Resources and 
Intergovernmental Relations Subcommittee on July 11, 1989 
revealed, the design, implementation and conclusions of the CDC 
study were so ill conceived as to suggest that political 
pressures once again interfered with the kind of professional, 
unbiased review Congress had sought to obtain.** 

The Agent Orange validation study, for example, a study of 



See 135 Congressional Record . Statement of Senator Tom 
Daschle (November 21, 1989); See also Agent Orange Hearings at p. 
37. 

** Qv^rgjiqht Pevjew of cpp's Agent Or?ipq? gtudy; Hgarj,nq 

Qggore tiie Human Resources and In tergovernmental Relatj,Qns 

Subcommittee of the Commi ttee on Government Operations House of 
Representatives . 101st Cong., 1st Sess. at p. 71 and 330 
(1989) [hereinafter cited as Agent Orange Hearing]. 

24 



349 



the long-term health effects of exposures to herbicides in 
Vietnam, was supposedly conducted to determine if exposure could, 
in fact, be estimated.*' After four years and approximately $63 
million in federal funds, the CDC concluded that an Agent Orange 
exposure study could not be done based on military records.^ 
This conclusion was based on the results of blood tests of 64 6 
Vietneun Veterans which ostensibly demonstrated that no 
association existed between serum dioxin levels and military- 
based estimates of the likelihood of exposure to Agent Orange." 
Inexplicably, the CDC then used these "negative" findings to 
conclude that not only could an exposure study not even be done, 
but that the "study" which was never even conducted proves that 
Vietnam Veterans were never exposed to harmful doses of Agent 
Orange. 

Even more disturbing, when the protocol for this "study" and 
the blood test procedures were examined further, there appeared 
to be a purposeful effort to sabotage any chance of a meaningful 
Agent Orange exposure analysis. For instance, the original 
protocol for the Agent Orange exposure study understandably 
called for subject veterans to be tracked by company level 



Id. at 37; see also . Protocol for Epidemiologic Studies 
of the Health of Vietnam Veterans, Centers for Disease Control, 
Public Health Service, U.S. Department of Health and Human Services 
(November, 1983). 

** Agent Orange Hearings at 13 (Statement of Dr. Vernon Houk) . 

" Id. at 12-13. 



83-529 95-12 



350 



location. By tracking company level units of 200 men, rather 
than battalions of 1,000 men, the location of men in relation to 
herbicide applications would be )cnown with greater precision, 
thereby decreasing the probeibility that study-subjects would be 
misclassified as having been or not been exposed to Agent Orange. 

However, in 1985 the CDC abruptly changed the protocol to 
have battalions, rather than companies, serve as the basis for 
cohort selection and unit location." By the CDC's own 
admission, changing the protocol to track veterans on the broader 
battalion basis effectively diluted the study for the simple 
reason that many of the 1,000 men in a battalion were probably 
not exposed to Agent Orange. Why then did the CDC change the 
protocol in 1985? 

According to Dr. Vernon Houk, Director of the Center for 
Environmental Health and Injury Control, the department within 
the CDC responsible for conducting the Agent Orange study, the 
protocol was changed because the CDC concluded that company- 
specific records were unreliable and contained too many gaps of 
information. As a result, military records could simply not be 



** Ifl. at 41. 

" Id. at 38. 

** Agent Orange Hearing: Testimony of Dr. Vernon Houk at 38- 
40 and 69. Dr. Houk sports an unbounded skepticism for the health 
hazards of dioxin. He recently endorsed the lessening of the dioxin 
dumping standard in the State of Georgia at a rate 500 times more 
lenient than EPA recommended guidelines. See Letter from Dr. 
Vernon N. Houk to Leonard Ledbetter, Commissioner Georgia 
Department of Natural Resources (November 27, 1989). 

26 



351 



Richard Christian, the former director of the Environmental 
Study Group of the Department of Defense ("ESG") testified that 
not only was this conclusion false, but that he had personally 
informed the CDC that adequate military records existed to 
identify company-specific movements as well as spray locations.*' 
Furthermore, in a February 1985 report to the Congressional 
Office of Technology Assessment, the CDC reported that in 
analyzing 21 of 50 detailed computer HERBs tapes developed by the 
ESG on company movements that it was possible to correlate the 
exposure data to areas sprayed with Agent Orange with consistent 
results.'" Indeed, a peer reviewed study sponsored by the 
American Legion conclusively demonstrated that such computerized 
data could be used to establish a reliable exposure 
classification system essential to any valid epidemiologic study 
of Vietnam Veterans.*' 

In addition to altering the protocol from company units to 
battalions, the CDC further diluted the study by changing the 
protocol on the length of time study subjects were to have served 
in Vietnam. Whereas the original protocol required subjects to 
have served a minimum of 9 months in combat companies, the CDC 
reduced the minimum to 6 months. Furthermore, the CDC eliminated 



Procedures and Statistical Issues. See also American Legion 
Magazine Special Issue, "Agent Orange" (1990) at p. 12. 

'^ Agent Orange Hearing 155-220 (Testimony of Steven and 
Jeanne Stellman) ; American Legion and Columbia University Vietnam 
Experience Study, Environmental Research (December, 1988). 



352 



from consideration all veterans who served more than one tour in 
Vietnam. Finally, while the original protocol called only for 
subjects who served in Vietnam from 1967 to 1968, the years that 
Agent Orange spraying was at its height, the CDC added an 
additional 6 months to this time period. The net effect of these 
various changes was seriously to dilute the possibility that 
study subjects would have been exposed to Agent Orange, which in 
turn would impair any epidemiological study's gdDility to detect 
increases in disease rate.*^ 

Although the above referenced problems cast serious 
suspicion on the work of the CDC, perhaps its most controversial 



" Agent Orange Hearing at 46-49. This "dilution effect" 
is considered the classic flaw in epidemiological study design. 
Most epidemiologists would try to optimize the chances of observing 
an effect by including, rather than excluding, the subjects who are 
most likely to have been exposed to the suspected disease causing 
agent. This statistical aOaility to observe an effect if one is 
present is generally referred to as the "statistical power" of a 
given study. 

When the CDC chose to generalize exposure to Agent Orange to 
groups of veterans who were less likely, rather than more likely, 
to be exposed, the power of the study was diluted. For example, 
if we assume that 1 out of every 5 men who served in Vietnam was 
exposed to Agent Orange, any possible effects of the exposure will 
be diluted when the 4 non-exposed men are averaged in. If we assume 
further that exposure to Agent Orange caused a doubling of the 
incidence of cancers among the 20% of men exposed, the effect would 
largely be obscured since 80% of the group being studied would not 
have been sprayed with Agent Orange and would thus have a normal 
background rate of cancer. Consequently, only exceptionally large 
increases in the cancer rate would be discovered and or reach 
statistical significance in a study group so diluted from the 
outset. See Agent Orange Hearing at 149 (Testimony of John F. 
Sommer, Jr. , Director National Veterans Affairs and Rehabilitation 
Commission the American Legion) . 

See also Agent Orange Legislation and Oversight: Hearing 
Before the Committee on Veterans' Affairs, United States Senate, 
100th Cong., (May 12, 1988) (Testimony of Dr. Joel Michalek) at pp. 
65, 66 and 668. 

28 



353 



action was to determine unilaterally that blood tests taken more 
than 20 years after a veteran's service in Vietnam were the only 
valid means of determining a veteran's exposure to Agent Orange. 
In addition, Dr. Houk further "assumed" that the half-life for 
dioxin in the blood was seven years. '^ when the underlying data 
for Houk's assumptions were recently reviewed, however, 11 
percent of the blood tests were invalid (i.e. study subjects had 
higher values of dioxin in their blood in 1987 than in 1982 even 
though the subjects had no known subsequent exposure to dioxin) 
and the half lives of dioxin in the remaining study subjects 
ranged from a low of 2 to a high of 740 years!** Yet despite 
this tremendous variance in the data and the high incidence of 
false results, Houk and the CDC concluded, rather remarkably, 
that a large scale exposure study was simply not possible since 
"negative" blood tests appeared to "confirm" that study subjects 
were not even exposed to Agent Orange. 

Such conclusions are especially suspect given the fact that 
scientists have consistently cautioned against the use of blood 
tests as the sole basis for exposure classification. Although 
blood and adipose tissue tests can be used to confirm that 



on a study of only 3 6 former Ranch Handers (members of "Operation 
Ranch Hand," the Air Force herbicide defoliation program) who had 
volunteered blood samples in 1982 and 1987. 

'* American Legion Magazine Reprint "A( 
also . Agent Orange Hearing at p. 67 (testimony of Dr. Houk revealed 
that the senior statistician on the Agent Orange project believed 
that the dioxin blood analysis was so flawed there is a substantial 
likelihood that there is no correlation between the exposure scores 
and the blood levels) . 

29 



354 



Vietnam ■ Veterans were heavily exposed to Agent Orange and the 
contaminant dioxin", even the CDC's own researchers have 
unequivocally stated that "much more has to be learned about the 
kinetics of dioxin metabolism and half-life before current levels 
can be used to fully explain historic levels of exposure."*' 

While the CDC's changes in protocol have been "justified", 
however unreasonably, on the basis of "scientific" 
explanations", what cannot be justified is the evidence of 
political interference in the design, implementation and drafting 
of results of the CDC study by Administration officials rather 
than CDC scientists. As early as 1986, the Subcommittee on 
Oversight and Investigations of the Committee on Energy and 
Commerce documented how untutored officials of the Office of 
Management and Budget (0MB) interfered with and second-guessed 
the professional judgments of agency scientists and 
multidisciplinazy panels of outside peer review experts 



Tissue of Agent Orange Exposed Vietnam Veterans and Matched 
Controls," 259 Jpymal Qf th? American M?cii<?e^3L A?soc;i?tj.on 1661 
(1988) . This report found that "Vietnam veterans who were heavily 
exposed to Agent Orange exceeded matched control subjects in both 
blood and adipose tissue levels of 2,3 ,7,8-tetrachlorodibenzo-p- 
dioxin (TCDD) but not in the levels of the 12 other 2,3,7,8- 
substituted dioxins and dibenzofurans that were detected. Since 
only TCDD among these compounds was present in Agent Orange but all 
are present in the population of the industrialized world, it is 
likely that the elevated TCDD levels arose from wartime exposure." 

** Patterson, "Levels of Polychlorinated Dibenzo-p-dioxins 
and Dibenzofurans in Workers Exposed to 2,3,7,8 
tetrachlorodibenzo-p-dioxin, 16 American Journal of Industrial 
Medicine 135, 144 (1989). 

'' See generally . Agent Orange Hearing (Testimony of Dr. 
Vernon Houk) at 44-50. 



355 



effectively to alter or forestall CDC research on the effects of 
Agent Orange, primarily on the grounds that "enough" dioxin 
research had already been done.** These Agent Orange Hearings 
revealed additional examples of political interference in the 
CDC's Agent Orange projects by members of the White House Agent 
Orange Working Group." 

Dr. Philip J. Landrigan, the former Director of the 
Environmental Hazards branch at the CDC, upon discovering the 
various irregularities in CDC procedures concluded that the 
errors were so egregious as to warrant an independent 
investigation not only of the methodology employed by the CDC in 
its validation study, but also a specific inquiry into what 
actually transpired at the Center for Environmental Health of the 
CDC." 

With these suspicio.is in mind, it should come as no surprise 
that those familiar with the CDC's work found little credence in 
the conclusions reached by the CDC in its recently released 
Selected Cancers Study. Even though the CDC has previously stated 
that it believes exposure to Agent Orange is impossible to 
assess, it found no difficultly in reporting to the press upon 
the release of the Selected Cancers Study that exposure to Agent 



Reduction Act; A Report Prepared for the Subcommittee on Oversight 
and Investigations of the Committee on Energy and Commerce, 99th 
Cong. 2nd Sess. (October 1986) . 



Houk) 



356 



Orange does not cause cancer. This conclusion was reached despite 
the fact that the CDC made no effort to determine, through 
military records or blood/adipose tissue tests, if study subjects 
were, indeed, exposed to dioxins; nor did the CDC attempt to 
verify exposure to Agent Orange of those study subjects who 
actually contracted cancerous diseases. In fact, according to 
scientists who have made preliminary reviews of the CDC's 
findings, the statistical power of any one cancer grouping, with 
the exception of non-Hodgkin ' s lymphoma, was so low as to make 
any conclusion virtually impossible. 

IV. RANCH HAND STUDY 

Unfortunately, political interference in government 
sponsored studies associated with Agent Orange has been the norm, 
not the exception. In fact, there appears to have been a 
systematic effort to suppress critical data or alter results to 
meet preconceived notions of what alleged scientific studies were 
meant to find.'^ As recently as March 9, 1990 Senator Daschle 
disclosed compelling evidence of additional political 
interference in the Air Force Ranch Hand study, a separate 
government sponsored study meant to examine the correlation 
between exposure to Agent Orange and harmful health effects among 
Air Force veterans who participated in Agent Orange spraying 



'^ See generally Agent Orange Hearing; Congress ional Record. 
S 2550 (March 9, 1990); Congressional Record . (November 21, 1989) 
(Statements of Senator Thomas Daschle) . 



357 



missions under Operation Ranch Hand. As Senator Daschle 

explained: 

In January 1984, the scientists in charge of the Ranch Hand 
Study issued a draft baseline morbidity report that 
described some very serious health problems in the Ranch 
Hand veterans and stated that the Ranch Handers, by a ratio 
of five to one, were generally less well than the veterans 
in the control group. The opening sentence of the draft 
report's conclusion was clearly stated: "It is incorrect to 
interpret this baseline study as 'negative.' " 

After the Ranch Hand Advisory Committee, which operates 
under the White House A^ent Orange Working Group of the 
Domestic Policy Council, got its hands on the document, the 
final report was changed in some very important ways. Most 
notably, the table and exposition explaining that the Ranch 
Handers were generally less well than the controls was 
omitted, and the final conclusion was altered substantially. 
The statement that the baseline study was not negative was 
completely omitted and the study was described as 
"reassuring." ^ 

By altering the study's conclusion, opponents of Agent 
Orange compensation were able to point to "irrefutable proof" 
that Agent Orange is not a health problem: if those veterans most 
heavily exposed to Agent Orange did not manifest any serious 
health problems, they argued, then it could safely be deduced 
that ne veteran allegedly exposed to Agent Orange in smaller 
doses could have health problems. Yet, when Senator Daschle 
questioned Air Force scientists on why discrepancies existed 
between an Air Force draft of the Ranch Hand Study and the final 
report actually released to the press, the answers suggested not 
merely disagreements in data evaluation, but the perpetration of 
fraudulent conclusions. In a word, the major premise was badly 

" See Congres sional Record S 2550 (March 9, 1990). 
33 



358 



flawed. 

For exzuBple, in 1987 Ranch Hand scientists confirmed to 
Senator Daschle that an unpublished birth defects report shows 
that birth defects among Ranch Hand children are double those of 
children in the control group and not "minor" as originally 
reported in 1984." 

This increase in birth defects takes on added significance 
when one considers that the original CDC birth defects study, 
which found no increase in birth defects, merely examined birth 
defects as reported on birth certificates, rather than as 
reported by the child's parent or physician. The CDC never 
recorded hidden birth defects, such as internal organ 
malformations and other disabilities that only became apparent as 
the child developed. Consequently, it is very likely that the 
CDC's negative findings on birth defects were also vastly 
understated." 

In addition to elevated birth defects, Ranch Handers also 
showed a significant increase in skin cancers unrelated to 
overexposure to the sun as originally suggested in the 1984 
report. Air Force scientists also admitted that Air Force and 
White House Management representatives were involved in 



" Congressional Record . (November 21, 1989) (Statement of 
Senator Thomas Daschle) . 

** The CDC birth defects study was confined to Vietnam 
Veterans located in the Atlanta, Georgia region. The study was not 
an Agent Orange birth defects study since no effort was made to 
determine whether the veterans had even been exposed to Agent 
Orange. See notes 10 and 18 supra for additional information on 
birth defects. 

34 



359 



scientific decisions in spite of the study's protocol which 
prohibited such involvement." 

On February 23, 1990, the Air Force released a follow-up 
morbidity report on the Ranch Handers. That report, "1987 
Followup Examination Results," described statistically 
significant increases in health problems among Ranch Handers 
including: all cancers — skin and systemic combined, both 
verified and suspected; skin cancers alone; hereditary and 
degenerative neurological diseases and other problems. The Air 
Force concluded, however, that these and other problems cannot 
necessarily be related to Agent Orange/dioxin exposure, as they 
do not always show a "dose-response" relationship - particularly 
since the exposure index used in the data analysis "is not a good 
measure of actual dioxin exposure." ** 

With this conclusion, the Air Force for the first time 
officially acknowledged that the conclusions reached in its 
original 1984 Ranch Hand study are not simply moot, but that the 
Ranch Hand study is not, at this date, an Agent Orange study at 
all since dioxin exposure could not be determined reliably in the 
first place. In other words, the Air Force could just as easily 
have concluded that the health problems associated with the Ranch 
Handers were not necessarily related to eating beer nuts. 



" Congressional Record . S 2551 (March 9, 1990) (Statement 
of Senator Daschle) . 

" Wolfe, et. al.. Air Force Health Study and Epidemiologic 
Investigation of Health Effects in Air Force Personnel Following 
Exposure to Herbicides (Feb. 1990) at p. vi. 



360 



For the Air Force to have made the statement in 1990 of no 
evidence of a link between exposure to Agent Orange and the 
cancer problems experienced by Ranch Handers is, as Senator 
Daschle notes, "patently false."*'. Although not yet conclusive, 
what the Ranch Hand and CDC studies demonstrate is that there is 
evidence of a link between health problems and dioxin exposures 
which may become definitive when a new and reliable exposure 
index is used to evaluate the data. 

As stated by Dr. James Clary, one of the scientists who 

prepared the final Ranch Hand report: 

The current literature on dioxin and non-Hodgkin ' s lymphoma 
and soft tissue sarcoma can be characterized by the 
following: 

1. It underestimates (reduced risk estimates) the 
effect of dioxins on human tissue systems. As 
additional studies are completed we can expect to see 
even stronger correlations of dioxin exposure and 
NHL/STS . 

2. Previous studies were not sensitive enough to detect 
small, but statistically significant increases in 
NHL/STS. As time progresses, and additional evidence is 
forthcoming, it will be increasingly difficult for 
anyone to deny the relationship between dioxin exposure 
and NHL/STS.*^ 

V. INDEPENDENT STUDIES 

Shamefully, the deception, fraud and political interference 
that has characterized government sponsored studies on the health 



" Congressional Record S. 2551 (March 9, 1990). gee a^sp 
Letter from Ma j . Gen James G. Sanders, U.S.A.F. Deputy Surgeon 
General to Senator Thomas Daschle (February 23, 1990). 

** Letter from Dr. James Clary to Senator Tom Daschle 
(September 9, 1988) . 



361 



effects of exposure to Agent Orange and/or dioxin has not escaped 

studies ostensibly conducted by independent reviewers, a factor 

that has only further compounded the erroneous conclusions 

reached by the government. 

For instance, recent litigation against the Monsanto 

corporation revealed conclusive evidence that studies conducted 

by Monsanto employees to examine the health effects of exposure 

to dioxin were fraudulent. These same fraudulent studies have 

been repeatedly cited by government officials to deny the 

existence of a relationship between health problems and exposure 

to Agent Orange. According to court papers: 

Zack and Gaffey, two Monsanto employees, published a 
mortality study purporting to compare the cancer death rate 
amongst the Nitro workers who were exposed to Dioxin in the 
1949 explosion with the cancer death rate of unexposed 
workers. The published study concluded that the death rate 
of the exposed worker was exactly the same as the death rate 
as the unexposed worker. However, Zack and Gaffey 
deliberately and knowingly omitted 5 deaths from the exposed 
group and took 4 workers who had been exposed and put these 
workers in the unexposed group, serving, of covurse, to 
decrease the death rate in the exposed group and increase 
the death rate in the unexposed group. The exposed group, in 
fact, had 18 cancer deaths instead of the reported 9 deaths 
(PI. Ex. 1464), with the result that the death rate in the 
exposed group was 65% higher than expected (emphasis in 
original) . 



Brief of Plaintiffs-appellees in Kemner. et. al. v. 
Monsanto Company . No. 5-88-0420 (5th Dist. , Illinois Appellate 
Court) (Oct. 3, 1989) (as the facts were proven at trial, the 
appeal only considered appealable matters of law). Plaintiff's 
brief refers to Zack and Gaffey, "A Mortality Study of Workers 
Employed at the Monsanto Company Plant in Nitro, WV," Human and 
Environmental Risks of Chlorinated Dioxins and Related Compounds 
(1983) pp. 575-591. It should be noted that the Advisory Committee 
classified this report as "negative" in evaluating compensation for 
NHL. 

The brief also states that another study of the workers 
exposed in the 1949 accident was also fraudulent (e.g. R.R. Suskind 

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Siallarly, recent evidence also suggests that another study 
heavily relied upon by those opposed to Agent Orange compensation 
to deny the existence of a link between dioxin and health effects 
was falsified. Three epidemiologic studies and several case 
report studies about an 1953 industrial accident in which workers 
at a BASF plant were exposed to dioxins concluded that exposure 
to TCDD did not cause human malignancies.^ A reanalysis of the 
data that comprised the studies, all of which was supplied by the 
BASF company itself, revealed that some workers suffering from 
chloracne (an acknowledged evidence of exposure to dioxin) had 
actually been placed in the low-exposed or non-exposed cohort 
groups. Additionally, 20 plant supervisory personnel, not 
believed to have been exposed, were placed in the exposed group. 

When the 20 supervisory personnel were removed from the 
exposed group, thereby negating any dilution effect, the 
reanalysis revealed statistically significant increases in 
cancers of the respiratory organs (lungs, trachea, etc.) and 



and V.S. Hertzberg, "Human Health Effects of 2,4,5-T and Its Toxic 
Contaminants," Journal o f the American Medical A ssociation. Vol. 
251, No. 18 (1984) pgs. 2372-2380.) The study reported only 14 
cancers in the exposed group and 6 cancers in th,e unexposed group. 
Trial records conclusively demonstrated, however, that there were 
28 cancers in the group that had been exposed to dioxins, as 
opposed to only 2 cancers in the unexposed group. 

"" See, e.g. Thiess, Frentzel-Beyme, Link, "Mortality Study 
of Persons Exposed to Dioxin in a Trichlorophenol Process Accident 
that Occurred in the BASF AG on November 17 , 1953", 3 American 
Journal of Industrial Medicine 179-189 (1982) 

38 



363 



conducted this study, "[t]his analysis adds further evidence to 
an association between dioxin exposure and human malignancy." 

Recent evidence also reveals that Dow Chemical, a 
manufacturer of Agent Orange was aware as early as 1964 that TCDD 
was a byproduct of the manufacturing process. According to Dow's 
then medical director. Dr. Benjamin Holder, extreme exposure to 
dioxins could result in "general organ toxicity" as well as 



Friedemann Rohleder, "Dioxins and Cancer Mortality 
Reanalysis of the BASF Cohort," presented at the 9th International 
Symposium on Chlorinated Dioxins and Related Compounds, Toronto, 
Ontario (Sept. 17-22, 1989). BASF recently published a study in 
an attempt to refute the allegations that the original studies 
related to the accident were fraudulent. See Zobier, Messerer & 
Huber, "Thirty Four Year Mortality Follow Up of BASF Employees, 62 
Occupational Environmental Health 139-157, (Oct. 19, 1989). While 
the company states that "there was no significant increase in 
deaths from malignant neoplasms," the study does conclude that: 

There was, however, a significant excess for all cancers 
combined among the chloracne victims 20 or more years after 
initial exposure when an excess would be most likely to occur. 
In addition, there is the notable finding on one case of liver 
cancer without cirrhosis in a worker with an exceptionally 
high level of TCDD in the blood. 

Id. at 155. See also id. at 139 ("In general, our results do not 
appear to support a strong association between cancer mortality and 
TCDD, but they do suggest that some hazard may have been 
produced. ") (emphasis added) and 149 ("Although TCDD blood levels 
were available for only 5 of the 10 subjects, the three highest 
levels were found in subjects with liver cancer, leucosis and 
Merkell-cell carcinoma of the skin."). 

^ Wanchinski, "New Analysis Links Dioxin to Cancer," New 
Scientist . (Oct. 28, 1989) p. 24. 

^ See L. Casten, Patterns of Secrecy: Dioxin and Agent 
Orange (1990) (unpublished manuscript detailing the efforts of 
government and industry to obscure the serious health consequences 
of exposure to dioxin) . 



364 



recent expert witness who reviewed Dow Chemical corporate ' 
documents on behalf of a plaintiff injured by exposure to dioxin 
who successfully sued Dow'* states unequivocally that "the 
manufacturers of the chlorphenoxy herbicides have known for many 
years about the adverse effects of these materials on humans who 
were exposed to them."" 

VI. CURRENT SCIENCE ON HEALTH EFFECTS OF HERBICIDES AND DIOXIN 

Despite its poor record in carrying out its responsibility to 
ascertain the health effects of exposure to Agent Orange, the CDC 
has been candid in some of its findings. As early as 1983, for 
instance, the CDC stated in the protocol of its proposed Agent 
Orange Studies "[t]hat the herbicide contaminant TCDD is 
considered to be one of the most toxic components known. Thus 
any interpretation of abnormal findings related to 2,4, 5-T must 
take into consideration the presence of varying or undetermined 



cert denied 110 S.Ct. 328 (1989) 



^ Letter from Daniel Teitelbaum, M.D., P.C. to Admiral E.R. 
Zumwalt, Jr. (April 18, 1990). Dr Teitelbaum additionally states: 

What I do think... may bear on the Agent Orange issue, is the 
fact that in review of Dow's 2,4-D documentation I found that 
there are significant concentrations of potentially 
carcinogenic materials present in 2,4-D which have never been 
made known to the EPA, FDA, or to any other agency. Thus, in 
addition to the problem of the TCDD which, more likely than 
not, was present in the 2, 4, 5-T component of Agent Orange, the 
finding of other dioxins and closely related furans and 
xanthones in the 2,4-D formulation was of compelling interest 
to me. 

40 



365 



amounts of TCDD." 

In 1987, after first being leaked by the New York Times , a VA 
mortality study was released indicating a 110 percent higher rate 
of non-Hodgkin ' s lymphoma in Marines who served in heavily 
sprayed areas as compared with those who served in areas that 



Also in 1987, a second VA study found a suggestive eight-fold 
increase in soft tissue sarcoma among veterans most likely to 



CDC Protocol, see note 1 supra . The CDC went on to state 
that a wide variety of health effects have been observed following 
the administration of TCDD to experimental animals including soft 
tissue sarcomas emd lymphoma, nasal and nasopharyngeal cancers, 
birth defects, changes in thymus and lymphoid tissues, and other 
numerous cancers. Additionally, the CDC acknowledged the toxic 
effects of occupational exposure to dioxin, including evidence that 
exposure "may be associated with an increased risk of soft tissue 
sarcoma and lymphoma" and perhaps nasal and nasopharyngeal cancers. 

"" Breslin, et. al. "Proportionate Mortality Study of U.S. 
Army and U.S. Marine Corps Veterans of the Vietnam War," Veterans 
Administration (1987). 

^ I^. Some scientists, including the Advisory Committee have 
attempted to denigrate these significant findings on the basis that 
Army personnel did not show similar results. The explanation for 
this lack of comparative Army findings is directly attributable to 
the dilution effect caused by including logistics personnel as part 
of the Army study. Marines were studied as a separate group. The 
Marine's logistical support personnel (i.e. the Navy), were not 
included. Thus, the increased cancers among Marines were clearly 
associated with field exposure to Agent Orange. 

The Army study, on the other hand, combined field personnel 
with personnel on logistics assignments who were unlikely to have 
been exposed to Agent Orange. As a result, the Army findings were 
drastically diluted. Additionally, Army personnel generally 
engaged the enemy and returned to base, whereas Marines 
consistently remained in areas presumably sprayed by Agent Orange 
to provide medical, health and engineering assistance to the local 
population. Such "pacification" efforts gave Marines additional 
opportunities to be exposed to dioxins. 



366 



have been exposed to Agent Orange. 

A proportionate mortality study of deaths in pulp and paper 
mill workers in New Hampshire from 1975 to 1985 showed that one 
or more of the exposures experienced by such workers (dioxin is a 
byproduct of pulp and paper production) posed a "significant 
risk" for cancers of the digestive tract and lymphopoietic 
tissues." 

Another case control study of farmers in Hancock County, 
Ohio, showed a "statistically significant" rise in Hodgkin's 
disease and non-Hodgkin ' s lymphoma. Although the study 
speculates that exposure to phenoxy herbicides may be the cause 
of such elevated cancers, the study recognizes that, given the 
size of its cohort, the only credible conclusion that can be 
drawn is that it "adds to the growing body of reports linking 
farming and malignant lymphoma, particularly NHL." '^ 

A study of disease and non-battle injuries among U.S. 
Marines in Vietnam from 1965 to 1972 showed a significantly 
higher rate of first hospitalizations for Marines stationed in 
Vietneun as opposed to Marines stationed elsewhere, particularly 



Kang, et. al., "Soft-Tissue Sarcoma and Military Service 
in Vietnam: A Case Control Study," 79 Journal of the National 
Cancer Institute 693 (October, 1987) . The increases were not 
statistically significant as reported. Nonetheless, the results 
are remarkable. 

" E. Schwartz, "A Proportional Mortality Ratio of Pulp and 
Paper Mill Workers in New Hampshire," 45 British Journal of 
Industrial Medicine. 234-238 (1988). 

'^ Dubrow, Paulson & Indian, "Farming and Malignant Lymphoma 
in Hancock County, Ohio," 4 5 British Journal of Industrial 
Medicine . 25-28 (1988) . 



367 



for neoplasms, diseases of the blood and blood forming organs and 
diseases of the circulatory and respiratory systems." Of 
particular significance is the fact that the rate of first 
hospitalization for disease and non-battle injuries among Vietnam 
personnel rose steadily, reaching a peak in 1969, while the rate 
of non-Vietnam personnel remained relatively constant." This 
rise in hospitalization for non-combat injuries coincides exactly 
with the increased use of Agent Orange, reaching a peak in 1969, 
and declining thereafter until its elimination in 1971. 

In a recently published article entitled "2,4-D, 2,4,5 -T, 
and 2,3,7,8 -TCDD: An Overview", the authors acknowledge that at 
least three weaknesses in research related to dioxins are 
sufficient to cast doubt on the validity of any study."* The 



Palinkas & Coben, "Disease and Non-Battle Injuries Among 
U.S. Marines in Vietnam, 153 Military Medicine 150 (March, 1988). 

^ I^. at 151. It should be noted that the year of greatest 
combat activity, as measured by the number of personnel wounded in 
action, 1968, had the smallest disease and non-battle injury vs. 
wounded in action ratio. Id. at 152. 

"* Lilienfeld and Gallo "2,4- 
An Overview," Epidemiologic Review . Vol. II (1989). Three major 
criteria must be considered in evaluating the numerous 
epidemiologic studies of phenoxy herbicides and 2, 3,7,8-TCDD: 1) 
the accuracy of exposure assessment; 2) the studies' statistical 
power; and 3) the adequacy of follow-up. Problems in any one of the 
three areas leaves the study open to criticism and subject to 
manipulation. 

For instance, in retrospective studies, various proxies of 
exposure to herbicides and 2, 3, 7, 8, -TCDD have been used such as 
military service in Vietnam or residence in an area in which the 
herbicides were sprayed. The weakness in such an approach is that 
unless the proxy corresponds to exposure, the "exposed group" is 
diluted with the individuals who have NOT been exposed, thereby 
reducing the magnitude of the strength of the association. In fact, 
such reduction may be of such a degree as to preclude detection of 
any effect. The authors note, however, that the recent development 

43 



368 



authors ■ report that while the data on soft tissue sarcoma and 
phenoxy acids are too inconsistent to allow for any comment at 
this time, there is evidence of a strong association between STS 
and the suspect chemicals in 2 of the 8 studies analyzed in their 
article. Furthermore, the birth defect studies analyzed "suggest 
that adverse reproductive effects can be caused by [dioxin]."'* 

Recent studies in Vietnam continue to show statistically 
significant reproductive anomalies and birth defects among women, 
and children of women presumably exposed to Agent Orange 



of a serum marker for 2,3,7,8-TCDD by Kahn may provide the means 
of identifying persons who have been exposed. 

Furthermore, studies concerning Agent Orange have nearly all 
been conducted in the past decade. This 10 year latency period is 
generally thought to be insufficient for many cancers to be 
clinically detected. 

"* See note 10 supra . It should be noted that as early as 
1977 information about Agent Orange's potential for genetic damage 
was known to the VA. For example, a "NOT FOR RELEASE" VA document 
expressly noted Agent Orange's "high toxicity" and "its effect on 
newborn, deformed children — similar to the thalidomide 
situation." See L. Casten, Patterns of Secrecy note 73 supra at 
Department of Veteran Affairs p. 4. Similarly, in March of 1980, 
Senator Tom Daschle and Rep. David Bonior received an anonymous 
memorandum written on VA stationery which stated: 

chemical agents 2,4,5-T and 2,4-D commonly known as Agent 
Orange and Agent Blue, are mutagenic and teratogenic. This 
means they intercept the genetic DNA message processed to an 
unborn fetus, thereby resulting in deformed children being 
born. Therefore, the veteran would appear to have no ill 
effects from the exposure but he would produce deformed 
children due to this breakage in his genetic chain. .. .Agent 
Orange is 150,000 times more toxic than organic arsenic. 

Id . See also Wolfe & Lathrop, "A Medical Surveillance Program for 
Scientists Exposed to Dioxins and Furans," Human and Environmental 
Risks of Chlorinated Dioxins and Related Compounds . 707-716 (1983) 

44 



369 



In the December 1, 1989, issue of Cancer . a study of the 
cancer risks among Missouri farmers found elevated levels of lip 
and bone cancer as well as nasal cavity and sinuses, prostrate, 
non-Hodgkin ' s lymphoma and multiple myeloma. Smaller elevations, 
but elevations nonetheless, were found for cancers of the rectum, 
liver, malignant melanoma, kidney and leukemia. According to the 
authors, evidence of the cause for the elevated risks for these 
illnesses "may be strongest for a role of agricultural chemicals, 
including herbicides, insecticides and fertilizers." '^ 

Both the U.S. Environmental Protection Agency (EPA) and the 
International Agency for Research on Cancer (lARC) have concluded 
that dioxin is a "probable human carcinogen." 

In a work entitled "Carcinogenic Effects of Pesticides" to 
be issued by the National Cancer Institute Division of Cancer 
Etiology, researchers conclude that while confirmatory data is 
lacking there is ample evidence to suggest that NHL, STS, colon, 
nasal and nasopharyngeal cancer can result from exposure to 
phenoxy herbicides. 

A just released case control study of the health risks of 
exposure to dioxins confirmed previous findings that exposure to 



(Proceedings of International Symposium on Chlorinated Dioxins and 
Related Compounds, Arlington, VA, October 25-29, (1981)). The 
article explains the possible mechanism for paternally transmitted 
birth defects. 

'^ Brownson, et. al. "Cancer Risks Among Missouri Farmers," 
64 Cancer 2381, 2383 (December 1, 1989). 

" Agency for Toxic Substances and Disease Registry, pp. 7,, 
61-68, 94 reprinted in Rachel's Hazardous Waste News # 173 (March 
21, 1990) 

45 



370 



phenoxyacetic acids or chlorophenols entails a statistically 
significant increased risk (i.e. 1.80) for soft tissue sarcoma." 

As recently as February 28, 1990 an additional study found 
that fanners exposed to various herbicides containing 2,4-D may 
experience elevated risks for certain cancers, particularly 
cancers of the stomach, connective tissue, skin, brain, prostate, 
and lymphatic and hematopoietic systems."^ 

This week a scientific task force, after reviewing the 
scientific literature related to the potential human health 
effects associated with exposure to phenoxyacetic acid herbicides 
and/or their associated contaminants (chlorinated dioxins) 
concluded that it is at least as likely as not that exposure to 
Agent Orange is linked to the following diseases: non-Hodgkin • s 
lymphoma, soft tissue sarcoma, skin disorders/ chloracne, 
subclinical hepatotoxic effects (including secondary 
coproporphyrinuria and chronic hepatic porphyria) , porphyria 
cutanea tarda, reproductive and developmental effects, neurologic 



Eriksson, Hardell & Adami, "Exposure to Dioxins as a Risk 
Factor for Soft Tissue Sarcoma: A Population-Based Case-Control 
Study," 82 Jo^^naJ. of 1;he Natjopjil, gjincer Jpstjtute 486-490 (March 
21, 1990). It should be noted that in this study the median latency 
for phenoxyacetic acid and chlorophenols exposure was 29 and 31 
years respectively, thereby suggesting that many of the veterans 
who are at risk have not yet manifested symptoms of STS. 

Blair, "Herbicides and Non-Hodgkin 's Lymphoma: New Evidence 
From a Study of Saskatchewan Farmers," 82 Journal of the National 
Cancer In stitute 575-582 (1990). 

46 



371 



effects and Hodgkin's disease. 

On the same day that this scientific task force reported a 
statistically significant linkage between exposure to the dioxins 
in Agent Orange and various cancers and other illnesses, the 
Environmental Protection Agency reported that the cancer risk 
posed by the release of such a "potent carcinogen" as dioxin in 
the production of white paper products is "high enough to require 
tighter controls on paper mills. "'^ 

CONCLUSIONS 

As many of the studies associated with Agent Orange and 
dioxins attest, science is only at the threshold of understanding 
the full dimension of harmful toxic effects from environmental 

In 



American Legion, Vietnam Veterans of America, and the National 
Veterans Legal Services Project, reported by McAllister, "Viet 
Defoliant Linked to More Diseases, Washington Post . May 1, 1990 at 
A8, col. 4. The report also found that there are other disorders 
for which there is evidence suggesting an association with exposure 
to Agent Orange, but for which statistically significant evidence 
is not currently available. Those diseases include: leukemias, 
cancers of the kidney, testis, pancreas, stomach, prostate, colon 
hepatobiliary tract, and brain, psychosocial effects, immunological 
abnormalities, and gastrointestinal disorders. 

'^ Weisskopf, "EPA Seeking to Reduce Dioxin in White Paper: 
Cancer Risk Said to Justify Mill Restrictions," Washington Post . 
May 1, 1990 at A8, col. 1. 

'^ A recent report in the Washington Post suggests that there 
is an inherent uncertainty in trying to measure the dangers posed 
by the chemicals humans eat, drink and breathe. Since human 
experimentation is impossible to assess the effect of varied doses 
of a chemical on human health, scientists are ultimately required 

47 



372 



fact, a whole new discipline - ianunotoxicology - has developed 
to explore further the effects of enviroranental chemicals on 
human health and to relate animal test results to humans.^ 

Immunotoxicology has established, however, at a minimum that 
at least three classes of undesirable effects are likely occur 
when the immune system is disturbed by environmental exposure to 
chemicals such as dioxin, including: 1) immunodeficiency or 
suppression; 2) alteration of the host defense mechanism against 
mutagens and carcinogens (one theory is that the immune system 
detects cells altered by mutagens or other carcinogenic trigger 
and destroys these cells. Thus, an impaired immune system may not 
detect and destroy a newly forming cancer) ; and 3) 
hypersensitivity or allergy to the chemical antagonist. Because 
of dioxin 's ability to be both an immunosuppressant and a 
carcinogen, as early as 1978 immunologists were suggesting that 
"[a] gents such as TCDD...may be far more dangerous than those 
possessing only one of these properties."" 

While scientists are not in agreement, some 
immunotoxicologists argue that one molecule of a carcinogenic 
agent, like dioxin in the right place and at the right time can 



to speculate or guess as to the health effects of a given chemical 
to the human body. See Measuring Chemicals' Dangers: Too Much 
Guesswork?" Washington Post . March 23, 1990. 

** Silbergeld & Gaisewicz, "Dioxins and the Ah Receptor," 
16 American Journal of Industrial Medicine 455, 468-69 (1989). 

" Inadvertent Modification of the Immune Response - The 
Effect of Foods, Drugs, and Environmental Contaminants; Proceedings 
at the Fourth FDA Symposium; U.S. Naval Academy (August 28-30, 
1978), p. 78. 

48 



373 



cause the human immune system to turn on itself, manifesting such 
breakdowns in the form of cancer. Indeed, even some courts have 
accepted this theory of causation in matters specifically related 
to exposure to dioxin." 

With additional evidence from Vietnam suggesting that Agent 
Orange contaminants have the aOaility to migrate away from actual 
spray locations via river channels and the food chain, the 
opportunity for a Vietnam Veteran to have been exposed to dioxin 
contaminant molecules increases significantly." 

It cannot be seriously disputed that any large population 
exposed to chemical agents, such as Vietnam Veterans exposed to 
Agent Orange, is likely to find among its members a number who 
will develop malignancies and other mutagenic effects as a result 
of being exposed to harmful agents. 

To be sure, decisions today with regard to the seriousness 
of Agent Orange health effects must be made while the science of 



** See Peteet v. Dow Chemical Co. . 868 F.2d 1428, 1433 (5th 
Cir. 1989) cert denied 110 S.Ct. 328 (1989). 

" See e.g. Schecter, et. al., "Levels of 2,3,7,8-TCDD in 
Silt Samples Collected Between 1985-86 From Rivers in the North and 
South of Vietnam," 19 Chemosphere . 547-550 (1989) (suggestive 
findings that the predominant dioxin isomer in Agent Orange has 
moved into downstream rivers in the South of Vietnam) ; 01 ie, et. 
al., "Chlorinated Dioxin and Dibenzofuran Levels in Food and 
Wildlife Samples in the North and South of Vietnam," 19 Chemosphere 
493-496 (1989) (food and wildlife specimens in South Vietnam had 
a higher relative abundance of 2,3,7,8-TCDD suggesting 
contamination from Agent Orange); Schecter, et. al. "Chlorinated 
Dioxin and Dibenzofuran Levels in Food Samples Collected Between 
1985-87 in the North and South of Vietnam," 18 Chemosphere 627-634 
(1989) (Agent Orange contaminants, specifically 2,3,7,8-TCDD found 
at relatively elevated levels in food and wildlife samples 15-25 
years after environmental contamination with compound in South of 
Vietnam) . 

49 



374 



imnunotoxicology is in its infancy. After having evaluated and 
considered all of the known evidence on Agent Orange and dioxin 
contaminants, it is evident to ne that enough is knovm about the 
current trends in the study of dioxins, and their linkage with 
certain cancers upon exposure, to give the exposed Vietnam 
Veteran the benefit of the doubt. 

This benefit of the doubt takes on added credence given two 
separate means for determining exposure to Agent Orange - 1) 
HERBS and Service HERBs tapes establishing troop location for 
conparison with recorded Ranch Hand spraying missions; and 2) 
blood testing from living veterans to ascertain elevated dioxin 
levels. The inexplicable unwillingness of the CDC to utilize 
this data has had the effect of masking the real increase in the 
rate of cancers among the truly exposed. There is, in my 
opinion, no doubt that had either of these methods been used, 
statistically significant increased rates of cancer would have 
been detected among the Veterans for whom exposure can still be 
verified. 

Since science is now able to conclude with as great a 
likelihood as not that dioxins are carcinogenic directly and 
indirectly through immunosuppression, and since a large 
proportion of those exposed to dioxin can be so ascertained, I am 
of the view that the compensation issue for sejrvice-related 
illnesses associated with exposure to Agent Orahge should be 
resolved in favor of Vietnam Veterans in one of the two following 
ways: 

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375 



COMPENSATI ON FOR SERVICE REIATED ILLNESSES 

Any Vietnam Veteran, or Vietnam Veteran's child who has a 
birth defect, should be presumed to have a service-connected 
health effect if that person suffers from the type of health 
effects consistent with dioxin exposure and the veteran's health 
or service record establishes 1) abnormally high TCDD in blood 
tests; or 2) the veteran's presence within 20 kilometers and 30 
days of a known sprayed area (as shown by HERBs tapes and 
corresponding company records); or 3) the veteran's presence at 
fire base perimeters or brown water operations where there is 
reason to believe Agent Orange have occurred. 

Under this alternative compensation would not be provided 
for those veterans whose exposure came from TCDD by way of the 
food chain; silt runoff from sprayed areas into unsprayed 
waterways; some unrecorded U.S. or allied Agent Orange sprayings; 
inaccurately recorded sprayings; or sprayings whose wind drift 
was greater than 20 kilometers. Predictably, problems generated 
by the foregoing oversights, the mass of data to be analyzed as 
claims were filed, and the known loss of many service records 
would invalidate many veterans' legitimate claims. 
Alternative ?: 

Any Vietnam Veteran or child of a Vietnam Veteran who 
experiences a TCDD-like health effect shall be presumed to have a 
service-connected disability. This alternative is admittedly 

51 



376 



broader than the first, and would provide benefits for some 
veterans who were not exposed to Agent Orange and whose 
disabilities are not presumably truly service-connected. 
Nevertheless, it is the only alternative that will not unfairly 
preclude receipt of benefits by a TCDD exposed Vietnam Veteran. 

Furthermore, this alternative is consistent with the 
Secretary's decision regarding the service-connection of non- 
Hodgkin's lymphoma, as well as legal precedent with respect to 
other diseases presumed by the Department of Veterans Affairs to 
be connected to one or more factors related to military service 
(i.e. veterans exposed to atomic radiation and POW's with spastic 
colon) . 
PRESUMPTIONS OF AGENT ORANGE R ELATED HEAL TH EFFECTS 

I have also given considerable thought to which health 
effects are to be presumed likelier than not to be related to 
TCDD exposure and therefore service-connected. Any such 
determination must be made in light of: 1) the review of the 
scientific literature, including animal studies where human data 
does not exist or has been manipulated; 2) the inappropriate 
processes of the Veterans Advisory Committee on Environmental 
Hazards; 3) the past political manipulations of Ranch Hand and 
CDC studies; and 4) the recent discoveries of manipulation by 
scientists hired by chemical manufacturers of dioxin contaminants 
to evaluate the potentially best epidemiological data concerning 
TCDD's effects on humans. 

My evaluation of the evidence has been made with just such 
52 



377 



considerations in mind. Additionally, I have conferred with 
several experts in the field. After evaluating all the evidence . 
and material of record . I am convinced that there is better than 
"an approximate balance of positive and negative evidence" on a 
series of Agent Orange related health effects. 

It can, in my judgment, be concluded, with a very high degree 
of confidence, that it is at least as likely as not that the 
following are caused in humans by exposure to TCDD: non-Hodgkin ' s 
lymphoma, chloracne and other skin disorders, lip cancer, bone 
cancer, soft tissue sarcoma, birth defects, skin cancer, lung 
cancer, porphyria cutanea tarda and other liver disorders, 
Hodgkin's disease, hematopoietic diseases, multiple myeloma, 
neurological defects and auto-immune diseases and disorders. 

In addition, I am most comfortable in concluding that it is 
at least as likely as not that liver cancer, 
nasal/pharyngeal/esophageal cancers, leukemia, malignant 
melanoma, kidney cancer, testicular cancer, pancreatic cancer, 
stomach cancer, prostate cancer, colon cancer, brain cancer, 
psychosocial effects, and gastrointestinal disease are service- 
connected . 

I have separated the two foregoing subsets subjectively 
only because there is somewhat more data to support the former 
than the latter. Nonetheless, immunological and toxicological 
theory supports both subsets and fully justifies, in my view, the 
inclusion of both subsets of the foregoing health effects in 
determining a service-connected injury. 

53 



378 



Such a resolution of the embarrassingly prolonged Agent 
Orange controversy would be on the order of decisions to 
compensate U.S. soldiers who, contracted cancer after exposure to 
radiation from atomic tests and U.S. soldiers involved, without 
their knowledge, in LSD experiments. With the scientific basis 
now available for it to be stated with confidence that it is at 
least as likely as not that various health effects are related to 
wartime exposure to Agent Orange, there is the opportunity 
finally to right a significant national wrong committed against 
our Vietnam Veterans. 

RECOMMENDATIONS 

1. That the Secretary undertake a prompt reevaluation of the 
compensation decision impacting on Vietnam Veterans exposed to 
Agent Orange in light of accumulating scientific evidence that 
discredits earlier "findings" of an insufficient linkage between 
dioxin contaminants in Agent Orange and rare disease, such as 
cancer illnesses. 

2. To the extent that the Secretary deems it necessary to 
use the Veterans' Advisory Committee on Environmental Hazards to 
assist in his reevaluation, the current members should be 
dismissed — having demonstrated a disturbing bias in their 
review to date of the scientific literature related to Agent 
Orange and dioxin — and new members should be appointed in 
accordance with Section G of the Veterans' Dioxin and Radiation 
Exposure Compensation Standards Act, including persons with 
recognized scientific and medical expertise in fields pertinent 

54 



379 



to understanding the health effects of exposure to dioxin. The 
Coomittee meeting currently scheduled for May 16th and May 17th 
should be cancelled. 

3 . That the Secretary in making his decision regarding Agent 
Orange compensation for Vietnam Veterans do so on the basis of 
his independent evaluation of the existing scientific and medical 
evidence on the health effects of exposure to dioxins, as 
cataloged and discussed in this Report, and in full recognition 
that the standard to be applied — as mandated by both Congress 
and the courts — requires the resolution of doubts as to a 
number of cancers linked to dioxins in favor of the Vietnam 
Veteran. 



APPENDIX 4.— WRITTEN QUESTIONS AND THE 
RESPONSES 



RESPONSES TO POST HEARING QUESTIONS CONCERNING 

THE AUGUST 5 HEARING BEFORE THE SENATE COMMITTEE ON 

VETERANS' AFFAIRS 



PREPARES BY 
CENTERS FOR DISEASE CONTROL AND PREVENTION (CDC) 



QUESTION: 

(1) CDC has tentatively concluded that the rate of birth defects 
among children of Persian Gulf veterans in Mississippi was not 
unusually high. This was based on a comparison with the rate of 
birth defects in the Atlanta metropolitan area. But urban 
centers tend to have higher rates of birth problems, because of 
poverty and lack of prenatal care. Why did CDC choose Atlanta as 
the coo^arison to the Mississippi veterans? 

RESPONSE: 

In November 1993, the Mississippi media reported an apparent 
increase in the number of birth defects, rare illnesses, and 
other health problems among children born to Persian Gulf War 
veterans from two Mississippi National Guard units. In December 
1993, the Department of Veterans Affairs, in collaboration with 
the Mississippi State Department of Health and the Centers for 
Disease Control and Prevention (CDC) , conducted a survey of these 
two National Guard units. The purpose of the survey was to 
assess the incidence of birth defects among children bom to 
selected Mississippi Guard members and to place this incidence in 
epidemiologic perspective based on available data on the rate of 
birth defects in the general population. The study was not 
intended to be a definitive case- control study. Rather, it was 
designed as a pilot survey to determine if a problem existed 
among a select group of veterans who had concerns that their 
Persian Gulf service had affected their children. Because of the 
limited scope of this survey, the results should not be 
generalized to all Persian Gulf veterans in Mississippi or 
nationwide. 

Of the 282 veterans who served in the two units in the Persian 
Gulf War, 254 (90 percent) were located and interviewed. Fifty- 
five children were conceived and born to 52 veterans after return 
from military service in the Persian Gulf; medical records were 
reviewed for 54 of the children. Three cases of major birth 
defects and two cases of minor birth defects were identified. 

To place the incidence of birth defects among children born to 
this select group of Persian Gulf War veterans into perspective, 
the investigators compared the observed rate of birth defects 
with the expected rate based on established birth defects, 

381 

83-529 95-13 



382 



surveillance systems and previous surveys. One of the 
surveillance systems used was the Metropolitan Atlanta Congenital 
Defects Program (MACDP) . 

MACDP, sponsored by CDC, the Emory University School of Medicine, 
and the Georgia Mental Health Institute, has maintained a 
population -based registry of children bom with congenital 
malformations since October 1967 and is one of the oldest such 
surveillance systems in the United States. 

This surveillance system represents births occurring in a five- 
county metropolitan Atlanta area which includes siiburban and 
urban areas. Approximately 40,000 births occur each year in the 
MACDP surveillance area. MACDP includes an active case 
ascertainment component. Data collection specialists visit 
hospitals to identify records of children with birth defects; 
follow-up is maintained from birth through the first year of 
life. 

The expected number of birth defects estimated from MACDP is 
similar to the number obtained from other comparaible surveillance 
systems, such as the California Birth Defects Monitoring Prograun 
and the Iowa Birth Defects Registry. Birth defects rates 
determined by a previous survey, the Collaborative Perinatal 
Project (CPP) , are generally higher than those obtained by the 
Atlanta, California, and Iowa systems. This is most likely due 
to CPP's protocol, in which each child was given a special 
excunination at birth and follow-up was continued for several 
years . 

Based on these population -based surveillance systems and the CPP 
survey, the rate for all major birth defects is estimated to be 
3 to 7 percent of live births. Applying this rate to the 
Mississippi study population, we would expect to see 2 to 4 major 
congenital defects; the investigators in the Mississippi study 
observed three. The rate for all minor birth defects combined is 
estimated to be 5 to 10 percent of live births. Based on this 
rate, 3 to 5 occurrences of minor birth defects would be expected 
in the Mississippi group of veterans; two were observed. Thus, 
compared to rates of birth defects observed in estadDlished 
surveillance systems and the CPP, the investigators in the 
Mississippi study concluded that there was no increase in the 
total number of birth defects observed cunong children bom to 
veterans from these two Mississippi National Guard units. 

Concern has been raised about the use of CDC's MACDP data to 
estimate the expected number of birth defects. One concern is 
that the rate of birth defects in urban areas may be higher than 
in the general population because of poverty and lack of prenatal 
care. Another concern is that veterans may represent a select 
population who would be expected to have a different rate of 
birth defects than the general population. Thus, some argue that 



383 



a comparison with urban rates may mask an increase in the rate of 
birth defects among the veteran group. 

Regarding the first concern, the number of birth defects observed 
in the Metropolitan Atlanta area is similar to the rate found by 
the birth defects surveillance prograun in Iowa, in which births 
occur in predominantly rural areas. Thus, based on two 
comparable surveillance systems, there does not appear to be a 
significant impact of urban status on an overall estimate of the 
rate of birth defects. 

Regarding the second concern, no definitive evidence exists to 
suggest that as a whole veterans have a different risk for giving 
birth to children with malformations than non- veterans. In a 
case- control study of births occurring in the Atlanta 
metropolitan area, veterans were found to have a similar risk of 
fathering babies with birth defects as did non- veterans.' 
Several studies have suggested that active -duty women may be at 
higher risk for adverse pregnancy outcomes, particularly low 
birth weight and preterm delivery, than comparable civilian 
women. ^'' In a CDC study of preterm delivery among 1,868 active- 
duty enlisted women, based on the experience of comparable United 
States women, the rate of preterm delivery was about 25 to 
45 percent greater than expected among white enlisted women and 
about 10 percent less than expected among black enlisted women. ^ 

The purpose of the Mississippi study was to conduct a rapid 
assessment of health problems among children born to a particular 
group of Persian Gulf War veterans. Such rapid assessments are 
very useful for determining if health problems are occurring at a 
greater than expected rate in relatively small groups with health 
concerns. Because of the small number of persons investigated in 
this survey, use of a local control group would have yielded very 
unstable estimates. A more formal case-control study with a 
large number of subjects, including active duty controls, would 
be required to conclusively rule out Persian Gulf service as a 
possible risk factor for adverse outcomes cimong children bom to 
military personnel. 

In summary, data from MACDP were utilized for comparison purposes 
because MACDP represents one of the few comprehensive birth 
defect surveillance systems in the United States; in fact, it is 
the oldest birth defects surveillance system in the United 
States. The rates of major and minor birth defects detected by 
this system are similar to the two other comprehensive birth 
defects surveillance systems in the United States. Given the 
stated purpose of the study, use of the Atlanta data was 
appropriate. 

1. Erickson JD, Mulinare J, McClain PW, Fitch GT, James LM, 

McClearn AB, Adams MJ. Vietnam veterans' risks for fathering 



384 



babies with birth defects. JAMA 1984;252:903-912. 

2. Buttemiller R. Prematurity among United States Air Force 
active-duty gravidas. Mil it Med 1984;149:665-668. 

3. Fox ME, Harris RE, Brekken AL. The active-duty military 
pregnancy: A new high-risk category. Am J Obstet Gynecol 
1977;129:705-707. 

4. Magann EF, Nolan TE. Pregnancy outcome in an active-duty 
population. Obstet Gynecol 1991;78:391-393. 

5. Adcuns MM, Read JA, Rawlings JS, Harlass FB, Samo AP, Rhodes 
PH. Preterm delivery among black and white enlisted women in 
the United States Army. Obstet Gynecol 1993;81:65-71. 



385 



QUESTION: 

(2) Many Persian Gulf veterans are concerned that their chronic 
Illnesses may be transmitted to family members. During the 
hearing we heard some very Interesting testimony about possible 
sexual transmission from "burning semen. * What can CDC do to 
evaluate the Incidence and prevalence of this problem among 
Persian Gulf War veterans? 

RESPONSE: 

The best method for assessing the self -reported incidence and 
prevalence of health problems among Persian Gulf War veterans, 
including the occurrence of problems such as painful intercourse 
or "burning semen, " is to conduct a survey that includes a 
representative sample of veterans who served in the Persian Gulf 
and veterans who served during the Gulf War but who were not 
deployed to the Gulf region. 

CDC is planning such a survey of Persian Gulf War veterans who 
listed Iowa as their home of record. The purpose of the Iowa 
study will be to assess the prevalence of self -reported adverse 
health outcomes among Iowa residents who were deployed to the 
Persian Gulf during Operation Desert Shield/Desert Storm and to 
compare this with the prevalence of adverse health outcomes among 
Iowa residents who served during the Persian Gulf War but who 
were stationed in locations other than the Gulf. In addition, 
there will be an assessment of pre-service, service, and post- 
service factors that may be associated with current health 
status. We anticipate that this assessment will serve as a model 
for State or local health departments and others for potential 
future assessments that may be undertaken by other Federal 
agencies. States, local governments, or universities. We expect 
that this survey will require 24 months to complete. 

The Defense Manpower Data Center has estimated that approximately 
20,500 Iowa residents served during the Gulf War; of these about 
8,000 served in the Gulf theater of operations of which 1,500 
were in the reserves or the National Guard. The Department of 
Defense can provide locating information for these veterans, 
including the last known address, social security number, and 
unit location during time of deployment. 

Based on preliminary estimates of sample size we anticipate that 
a randomly selected cohort of approximately 2,000 veterans who 
served in the Gulf and another 2,000 veterans who were stationed 
elsewhere during the Gulf War will be asked to participate. We 
will include in the assessment both men and women veterans who 
were on active duty, reservists, and in the National Guard during 
Operation Desert Shield/Desert Storm. Because of the large 
number of veterans that will be involved, we anticipate 
collecting data through a telephone survey. Criteria for 



386 



inclusion in the study include listing Iowa as the home of record 
and military service during the Persian Gulf War. 

We have been in contact with other researchers involved in 
studying the health of Persian Gulf veterans and researchers who 
were involved in studying Vietnam veterans with similar 
experiences. We are collecting questionnaires and instrument 
protocols from these investigators to ensure compareUaility of the 
Iowa survey with other ongoing research. In addition to 
questions cQsout the veterans' health, we amticipate including 
questions about the health status of faunily members, including 
questions on reproductive outcomes. 

In developing this study, we are mcdcing a concerted effort to 
seek input from affected veterans to ensure that we are 
addressing their concerns, including concerns about their 
reproductive health. We have met with representatives from local 
veterans' service organizations and will continue to seek their 
input as this study progresses. We view reports from veterans, 
such as those presented at the hearing, as an important source 
for crafting appropriate questions for the questionnaire. 



387 



QUESTION: 

(3) Is there a potential piibllc health risk from Persian Gulf 
War veterans who donate blood? 

RESPONSE: 

Leishmaniasis is a protozoan parasitic infection transmitted 
through the bite of an infected sand fly. Since leishmaniasis is 
endemic in Saudi Arabia, Kuwait, and other Southwest Asian 
countries, service men and women who seirved in the Persian Gulf 
region were at risk for contracting this disease. 

In November 1991, U.S. blood-banking organizations announced a 
ban on accepting blood from donors who had served in the Persian 
Gulf region because of concern aJsout possible bloodbome 
transmission of leishmaniasis. Announcement of this ban raised 
consciousness about leishmaniasis among health care personnel and 
lay persons, many of whom called CDC with questions sibout the 
disease. An article published in February 1992 in CDC's 

M(?ybi<;^itY an<^ M(?rt»3.?.ty weeHj.y Report described cases of 

leishmaniasis that had been identified in persons who had served 
in the Persian Gulf region.' 

As of November 1993, only 29 of more than 500,000 Desert Storm 
troops were reported as having leishmaniasis.' The incubation 
period for leishmeuiiasis is typically less than 18 months. 

In January 1993, the American Association of Blood Banks (AABB) 
lifted the ban on blood donations from persons who served in the 
Persian Gulf. According to Arthur J. Sivergleid, M.D., President 
of AABB, no documented cases of transfusion- transmitted 
leishmaniasis were found during the 14 months of the ban. The 
AABB recommendation to lift the ban was made with the assurance 
that routine health history questioning, undergone by all blood 
donors, will be sufficient to disqualify individuals with 
possible symptoms of leishmaniasis to ensure that the blood 
supply is safe from the disease.' 

Other than the already recognized risks associated with blood 
donations, CDC is not aware of other potential public health 
risks resulting from Persian Gulf War veterans who donate blood. 

1. CDC. Viscerotropic leishmaniasis in persons returning from 
Operation Desert Storm - 1990-1991. MMWR 1992;41:131-134, 

22. Ohl CA, Malone JD, Hyams KC, Oldfield E. Leishmaniasis among 
Desert Storm veterans: A diagnostic and therapeutic 
dilemma. Mil it Med 1993;158:726-729. 

(. Cotton P, Marwick C, Gunby P. Desert Storm veterans now may 
donate blood; Others call for discussion of donor tests. 
JAMA 1993;269:451-452. 



388 



QtTKSTION: 

(4) If a veteran is concerned that his or her future children 
may have birth defects or serious Illnesses because of the 
veterans' toxic exposures, how can he or she get accurate 
Information to answer those concerns? Who could they contact at 
your agency for such Information? 

The Division of Birth Defects and Developmental Disabilities, 
National Center for Environmental Health, Centers for Disease 
Control and Prevention, works with State health departments, 
academic institutions, and non-profit organizations to monitor 
the incidence of birth defects, conduct studies to determine 
causes of birth defects, and plan prevention programs for birth 
defects when causes are known. Unfortunately, the causes of over 
75 percent of all birth defects are still unknown. This makes it 
very difficult to provide the answers that veterans and other 
parents are so desperately seeking. 

If a veteran is concerned that his or her future children may 
have birth defects or serious illnesses because of the veteram's 
Persian Gulf service, he or she should contact a physician who is 
a specialist in birth defects. These specialists will most 
likely be found in the genetics departments of large medical 
schools. The veteran, or preferably the veteran's physician, may 
call the Division of Birth Defects euid Developmental Disabilities 
at (404) 488-7160. The Division does not provide clinical 
services, but does provide information to both physiciems and the 
general public on known reproductive hazards and risk factors for 
birth defects . CDC scientists can explain what is known and what 
remains unJcnown about the causes of birth defects . 



WRITTEN QUESTIONS FROM CHAIRMAN ROCKEFELLER TO 
DEPARTMENT OF DEFENSE AND THE RESPONSES 





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M,2A 1 



Reproductive Hazards and Military Service 



Question: In their report, GAO concluded that DoD 
made virtually no efforts to warn Gulf War service 
members that pesticides, decontaminants , and other 
widely used chemicals could harm their ability to have 
children. Do you have any explanation for that 
failure? 

Answer: The Department of Defense (DoD) used 
pesticides in the Gulf War that were registered for 
use by the Environmental Protection Agency (EPA). 
Under the Federal Insecticide, Fungicide, and 
Rodenticide Act, EPA requires that companies wanting 
to register pesticides must submit required testing 
data to EPA for review. Only after reveiw of the 
submitted data does EPA register the pesticide. EPA's 
reviews data from acute and subacute toxicology 
studies, long-term chronic feeding studies, and 
oncogenicity, teratogenicity, and mutagenicity, and 
reproductive effects studies. The pesticides used by 
the DoD are the same pesticide products that are used 
in the United States by public health agencies, the 
pest control industry, and by American citizens for 
pest control around their homes. If the EPA suspends 
or cancels the use of registered pesticide, the DoD 
ceases to use those pesticide products. In the Gulf 
War, the DoD did not use any suspended or canceled 
pesticides and, therefore, saw no reason to issue a 
warning to service members. 

Question: What will you do to make sure that DoD 
warns service members deployed to Rwanda, Zaire, or 
anyplace else, concerning the exposure to pesticides, 
decontaminants, and other widely used chemicals could 
harm the service member's ability to have children? 

Answer: The Joint Chiefs of Staff have been 
directed to ensure that all deployed personnel are 
apprised of potential environmental health hazards and 
are instructed on methods to protect themselves from 
occupational and environmental illnesses inherent in 
an area of operation(s) . DoD is aware that aggressive 
action is necessary to identify potential hazards, 
collect exposure data, document any training, and the 
use of protective and other preventive measures. 

An initial trial of the above principles was put 
in place for the operation "Restore Hope" deployment 
to Rwanda/Zaire/Uganda. The program has three major 



Reproductive Hazards and Military Service 



components: Tri-Service individuals at risk are 
identified, specific exposure data are being complied, 
and Health assessments conducted. Each of the major 
components has a pre-deployment, an operational, and a 
post-deployment phase. Although this initial trial is 
focused on the immediate requirements, it is our goal 
to move quickly toward prevention. In fact, troops 
sent on the most recent deployment to Haiti were given 
specific instructions and appropriate interventions 
regarding potential infectious and environmental 
hazards. 



Question: How will you make sure that U.S. 
troops are given and understand the information that 
is available in government manuals? 



Answer: Each Service has either a preventive 
medicine unit or a military public health section that 
conducts pre-deployment briefings. The briefings 
include a comprehensive health threat assessment. 
Country specific disease threat analyses are also 
available from the Armed Forces Medical Intelligence 
Center and the Armed Forces Pest Management Board. In 
addition to these pre-deployment briefings, a country- 
specific booklet is issued to each service member as 
part of a pre-deployment preparation agenda. The 
booklet serves as a ready reference concerning health 
threats and the required preventive measures. During 
an actual deployment. Preventive Medicine Teams, 
Environmental Health Teams, and/or Military Public 
Health Teams continuously evaluate health threats and 
devise both outbreak control, as well as prevention 
measures. Since the Preventive Medicine Teams, 
Environmental Health Teams, and Military Public Health 
Teams are in the Theater of Operation(s) with the 
deployed troops, immediate health related information 
is always available. 



391 



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AfMOPMIATIOM COMMITTII 
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OtHtR 

VETKRANS- AFFAIRS 



Reproductive Hazards and Military Service 



Question: During the hearing, we heard some very 
compelling testimony about the sexual problems that 
some Gulf War serviceman and their wives are having. 
These problems seem to be related to something in the 
veterans' semen, which could possibly be causing birth 
defects. According to scientists, the semen should be 
tested for pesticides, heavy metals, or other 
abnormalities. And yet, one of our witnesses, Kelli 
Albuck, told us that the military hospitals refuse to 
do the necessary tests to find out what's wrong. 
Since our hearing, what efforts has DoD made to ensure 
that military medical facilities will do this testing? 

Answer: The Department has been, and will 
continue to be responsive to reproductive health 
concerns of Gulf War veterans. To date, military 
health care providers have not reported any clusters 
of reproductive health problems among Gulf war 
veterans. The Centers for Disease Control and 
Prevention investigated a reported cluster of Gulf War 
related birth defects and health problems involving 
children of Guard members in Mississippi, but found no 
evidence of increased risk. 

The most common outcome measures in semen 
studies are sperm counts, sperm velocity, and 
percentage of motile, viable, and morphologically 
normal sperm. With respect to reproductive effects, 
biologic markers might be sought in semen; however, 
these types of tests are not widely available. The 
Department encourages Gulf War veterans and their 
spouses to present to military medical treatment 
facilities (MTFs) for care. MTFs should generally be 
capable of obtaining semen assays, analysis of sperm 
morphology, and hormonal studies when clinically 
indicated based on history and physical examination. 
These tests have proven quite useful in assessing 
agents reported to affected male reproductive 
capacity. 

In recognition of the need to sponsor additional 
research in reproductive health outcomes, several 
studies are planned to assess the impact of the Gulf 
War on reproductive function include: a comparison of 
pregnancy outcomes between Gulf War veterans and non- 
Gulf War veterans; an assessment as to whether Gulf 
War women or men have lower rates of fertility than 
active duty men or women who did not serve in the Gulf 
War; and, a study to determine whether there has been 



392 



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Reproductive Hazards and Military Service 



a higher rate of miscarriage among wives of men who 
deployed to the Gulf compared to non-veterans. 

Question: According to GAO, the Navy Medical 
Research Center in San Diego will conduct a study of 
birth outcomes of Gulf War veterans. Unfortunately, 
they will exclude Reserve units, even though they have 
a high proportion of Gulf War syndrome complaints. 
Shouldn't reserve units be included in this study? 

Answer: After careful review, the Navy Medial 
Research Center has decided to include a sample of 
individuals not currently on active duty to determine 
if that group is different from an active duty 
population. Additionally, the protocol entitled, 
"Gulf War Exposure Effects on Fertility and 
Miscarriage" will comprise two large populations. The 
study population will be all Service personnel who 
served in the Gulf War theater (n-696,000) and a 
random sample of service personnel who did not serve 
in the Gulf War theater (n=700,000). These studies 
should address the initial hypothesis of any Gulf War 
effect and will help to define specific areas for 
further research. 

Question: GAO also pointed out that infertility 
and miscarriage will not be included in the Navy 
study. Don't you agree that this is important 
information that should not be omitted? 

Answer: A study entitled, "A Comparative Study 
Of Pregnancy Outcomes Among Gulf War Veterans (male 
and female) and Other Active Duty Personnel" has 
begun. Also, a study entitled, "Gulf War Exposure 
Effects on Fertility and Miscarriage" has been 
proposed and is awaiting funding. Both these studies 
will address our concerns regarding the potential 
effects of the PGW on infertility and miscarriage. 



Question: Many military families use non- 
military hospitals for the birth or care of their 
children, especially if they Icnow they will have a 
child with birth defects. Will those families be 
included in the survey? 

Answer: Yes. 



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Q-5,6,7 1 



Reproductive Hazards and Military Service 



Question: What is the rate of major and minor 
birth defects for children born to military personnel 
in the Army, Navy, and Air Force? Is it higher in any 
of these individual services than the national 
average? 

Answer: Although the Defense Medical Information 
System has calculated a Military Health Services 
System infant mortality rate for FY88-FY90, I am not 
aware of a military birth defects surveillance system. 
However, CDC ' s national Birth Defects Monitoring 
Program may provide a source for background incidence 
rates for comparing adverse birth outcomes between 
Gulf War Veterans and an appropriate control group. 
CDC is currently collaborating on two such studies, 
one using the Mississippi State Birth Defects 
Registry and the other study involving Iowa military 
service members. 



Question: Does the Armed Forces Epidemiology 
Board have data on reproductive diseases including 
infertility, miscarriages, and birth defects for all 
members in our Armed Services? 

Answer: The Armed Forces Epidemiology Board 
(AFEB) does not maintain data on reproductive 
diseases, infertility, miscarriages and birth defects 
for all members of the Armed Services. The AFEB 
consists of a panel of civilian expert consultants who 
provide scientific medical advice and recommendations 
concerning the Services ' operational programs and 
policy and research concerning technological and 
epidemiological principles in the control of acute and 
chronic diseases. Although the Services have made 
presentations to the AFEB concerning reproductive 
issues, the AFEB does not maintain a central data base 
for this type of information. 

Question: If a healthy PGW service member 
experiences a miscarriage or stillbirth, or has a 
child with birth defects or who dies during infancy, 
is that information included in a PGW registry? 

Answer: Each service member participating in the 
Comprehensive Clinical Evaluation Program (CCEP) 
receives a thorough history and physical examination. 



394 



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. 1994 








Q-7(C0NT). 8 



Reproductive Hazards and Military Service 



Individuals who report a miscarriage or stillbirth as 
part of their medical history would have this 
information recorded in their medical records for 
inclusion in the CCEP data repository. 

The Department is planning several research 
studies which will review miscarriage/spontaneous 
abortions, and infertility data to allow us to 
estimate rates of these events in Gulf War veterans 
compared to personnel who did not deploy to the Gulf. 

Question: The U.S. Army Environmental Hygiene 
Agency conducted a study on U.S. military personnel 
who were sent from Germany to Kuwait to fight oil 
fires. They found genetic changes in these soldiers. 
What can you tell us about those results? I asked DoD 
for this report several months ago. When can our 
Committee expect to receive a copy of the entire 
study? 

Answer: The Biologic Surveillance Initiative was 
a companion study to the Kuwait Oil Fire Risk 
Assessment to quantify exposure to environmental 
contaminants by measuring biological markers of 
exposure and internal dose in DoD troops [11th Armored 
Cavalry Regiment(llth ACCRA) who deployed from Germany 
to Doha, Kuwait (within approxiioately 20 miles of the 
fires) soon after the war. 

Assay results of blood for sister chromatid 
exchange (SCE) frequency were consistent with an 
increase in genie stress for soldiers both during and 
after deployment to Kuwait. Increases in SCE 
frequency have been associated with many different 
chemicals and drug exposures, but they have not been 
determined to be predictive of or associated with any 
adverse health effect. Further study of genotoxic 
changes associated with deployments in general may be 
needed. 

The Kuwait Oil Fire Risk Assessment Report is 
being circulated within the Department and to other 
federal agencies for comment. The report should be 
available for release in the near future. 



395 



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HEARINO DATE 

AUGUST 5, 1994 


TdANSCBlfT PAGE NO. 




1 



Reproductive Hazards and Military Service 



Question: We have received data from DoD that 
show increased blood levels of several metals, 
including lead and cadmium, in U.S. military personnel 
who died in Kuwait during the Persian Gulf War. Heavy 
metals can cause birth defects or chronic illnesses 
such as those observed in the veterans who testified 
at the hearing. Did the DoD measure heavy metals in 
other military personnel who served in the Persian 
Gulf to determine if excessive exposure to heavy 
metals occured? 

Answer: The metals in the blood specimens of 
autopsy materials from veterans deployed to Kuwait and 
Saudi Arabia do not show a pattern consistent with 
exposure to heavy metals. From the Dover autopsies, 
the lead (PB) levels in only nine (9) of 53 patients 
were in excess of currently accepted action levels for 
children (lOOppb or lOug/dL) . Two (2) of these nine 
values were only slightly above lOOppb. Toxic effects 
of lead have been noted in the 900-1400ppb range, and 
deaths by lead poisoning have been accon^anied by 
levels in the 1000-5000ppb range. There were no 
histolopathologlc signs of lead poisoning, and it is 
probable that the few relatively high values are the 
result of contamination. For cadmium, many of the 
measured values were higher than expected, 31 of 50 
specimens were in excess of lOppb. Reference values 
generally range from .4 to 4.0ppb, although heavy 
smokers have been reported to average as high as 
e.Oppb. Smoking histories of the victims were not 
available, although this information alone could not 
account for some of the very high levels. As in the 
case of lead, there were no histopathologic findings 
consistent with cadmium toxicity. Contamination of 
the specimens from their containers or laboratory 
handling procedures seems more likely than are 
environmental exposures . 

Question: GAO listed 21 products used in the 
Gulf War that could have harmed reproductive function 
in Military personnel. What research is DoD planning, 
to determine whether men and women actually were 
harmed by using those products? 

Answer: Although the 21 chemicals may well be 
associated with adverse reproductive outcomes, 
establishing actual exposure levels is extremely 



396 



INSERT FOR THE RECORD | 




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AfraOMIIAriON* COMMITTCt 










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HEAKINO OATe 

AUGUST 5, 1994 




LINE NO. IINtlRTNO. 


a.-jpsoomju.\i 



Reproductive Hazaeds and Military Service 



difficult. Instead of basic chemical research, DoD 
has chosen an epidemiological approach. Our goal is 
to identify risk factors using epidemiological 
principles and then, if indicated, toxicological 
research can begin. Following this philosophy, the 
Assistant Secretary of Defense for Health Affairs 
[ASD(HA)] has established the Comprehensive Clinical 
Evaluation Program (CCEP) which will provide extensive 
medical examinations to Persian Gulf War veterans and 
their family members who are experiencing unexplained 
illnesses that they believe are related to the Persian 
Gulf War. The overall objective of the CCEP is to 
catalog, as well as is possible, the risk factors of 
the unexplained illnesses being experienced by 
veterans and their families. 

Question: GAO pointed out that DoD should gather 
information about fertility and miscarriages before 
soldiers are deployed, so that comparisons can be made 
after a war. That way, DoD would have accurate 
information about certain problems that were likely to 
be service related. Has DoD considered gathering such 
baseline information? 

Answer: Even under ideal conditions, 
reproductive outcome surveillance systems are 
extremely difficult to initiate and expensive to 
maintain. Specific case definitions are also 
difficult to formulate and valid exposure data 
difficult to obtain. Even with an extensive 
epidemiologic approach, the ability to obtain quality 
reproductive outcome data is arduous and complex. 
Despite its methodological problems, an 
epidemiological approach is the only logical way to 
compare fertility and miscarriage information among 
those who are deployed versus those who do not deploy 
versus a compareible U.S. civilian population. It 
would be inefficient and unnecessarily expensive to 
maintain reproductive information on all Service 
members in order to perform prospective studies. A 
much preferred method to logically consider a possible 
association between a deployment and a miscarriage or 
fertility problem is to perform retrospective 
epidemiologic analyses. Once the study population and 
an appropriate comparison population are assembled, a 
retrospective analysis could focus on specific 
hypotheses. Concerning fertility and miscarriages. 



397 





INSERT FOR THE RECORD 


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J-IKCONT), 12 



Reproductive Hazards and Military Service 



although methodologically complex, a retrospective 
approach offers the most logical solution. 

Question: Please provide detailed information 
about the pesticides and insecticides that were 
distributed to U.S. troops in the Persian Gulf War. 



Answer: A list of quantities of pesticides 
ordered for and returned from Operation Desert Shield 
and Desert Storm through the federal supply system is 
attached. Although we do not have actual records of 
use of these pesticides, these supply records provide 
an accounting of the specific pesticide and 
insecticide products that were available for use for 
disease-vector and pest control during the Persian 
Gulf War. 

These pesticides were primarily used by DoD 
personnel who were trained and certified in the proper 
and safe use of pesticides under the supervision of 
these personnel. The Department of Defense (DoD) 
trains and certifies these pesticide applicators by a 
plan approved by the Environmental Protection Agency 
(EPA) under the Federal Insecticide, Fungicide, and 
Rodenticide Act. (FIFRA). DoD pesticide applicator 
training meets or exceeds in quantity and quality that 
required for similar state training and certification 
plans under FIFRA. These individuals were taught that 
pesticides are to be applied according to the EPA 
label for use. 

A limited number of pesticides were actually 
issued or supplied to U.S. troops in the Gulf War. 
Military units issued repellents with instructions for 
use for personnel protection to service members. 
These were EPA registered repellents that service 
members used, when needed, to protect themselves from 
potentially disease transmitting mosquitoes or 
sandflies. The primary repellents issued to U.S. 
personnel for personnel protection were 33% Deet (N,N- 
diethyl-m-toluamide) cream that is applied to exposed 
skin and 0.5% permethrin aerosol for application to 
the battle dress uniform. Used together, these 
repellents prevent insect bites to the exposed skin 
and through the battle dress uniform. 

Applied as needed, the skin repellent is 
effective up to 12 hours. Permethrin was applied by 
spraying the outside of the battle dress unifojnn. The 
uniforms were not worn until the repellent application 



INSERT FOR THE RECORD 



APrROmiATIONS COMMirrtE 



HCARINO DATE 

AUGUST 5. 199A 



iTnANSCmPTPAOENO. LINiNO. 



ARMED tERVICU I 



X|MNATI VETERANS' AFFAIRS 



Reproductive Hazards and Military Service 



was completely dry. Regarding the use of these 
repellents, Deet has been used since 1957 by 50 to 100 
million people per year. Besides the registration of 
permethrin by EPA, the Food and Drug Administration 
approved the use of permethrin products for head lice 
and scabies control on human skin. 



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^ i UNITED STATES ENVIRONMENTAL PROTECTION AGENCY 

WASHINGTON, D.C. 20460 



W 



SEP 3 1994 



Honorable John D. Rockefeller tV 

Chairman 

Committee on Veterans' Affairs 

United States Senate 

Washington, D.C. 20510-6375 

Dear Mr. Chairman: 

Enclosed are responses prepared by the Office of Research and Development 
to the questions you sent to William H. Farland, Director, Office of Health and 
Environmental Assessment, on August 1 7, 1 994 following his appearance before the 
Committee on August 5, 1994 to testify concerning health risks related to military 
service. 

If I can be of further assistance, please let me know. Please contact Ken Wood 
of my staff on 202-260-5429 concerning the enclosed responses. 



Sincerely, 



Thomas C. Roberts 

Director 

Legislative Analysis Division 




Enclosure 



PrirfienRtcrdtiPapt 



408 



RESPONSES TO SENATOR ROCKEFELLER 

FOLLOWING UP ON THE AUGUST 5, 1994 HEARING 

ON DIOXIN EXPOSURE 



QUESTION 1: 

What data are available that suggest that a father's exposure to dioxin might 
result in increased birth defects, diseases, or learning disorders in offspring? 

ANSWER 1: 

There are no data to suggest that paternal exposure to dioxin might result in 
increased adverse effects in offspring. 



QUESTION 2: 

What are the implications of EPA's review of dioxin research for Vietnam 
veterans? 

ANSWER 2: 

Because EPA's reassessment of dioxin health effects evaluates all available data 
on this class of compounds, and because it posits a unifying mechanism of action for 
dioxin and related compounds, EPA's review will be important in characterizing 
hazards and risks for both cancer and non-cancer effects for 2,3,7,8-TCDD exposed 
veterans. It will also allow Vietnam experience exposures to be evaluated in 
comparison to the exposure to dioxin and related compounds which each of us incurs 
in our everyday lives in industrialized countries. The EPA has worked and will 
continue to work with the National Academy of Sciences' Institute of Medicine (lOM) 
as they evaluate data on, and the implications of, herbicide exposure during the 
Vietnam experience. The EPA's reassessment will no doubt be a valuable resource 
to the lOM. 



409 



QUESTION 3: 

What role does EPA have in assisting the DoD to predict and monitor 
reproductive hazards in the military? 

ANSWER 3: 

EPA plays an important role in predicting reproductive hazards for the DOD and 
other Federal agencies as well as the general public. EPA publishes widely-used 
guidance on the assessment of reproductive effects; carries out chemical-specific 
assessments for pesticides and other toxic substances which have wide applicability 
in hazard identification and labeling; and disseminates hazard and risk information on 
nationally available data systems for both military and non-military use. EPA plays a 
smaller role in monitoring for reproductive effects. Although EPA has conducted a 
few research programs which carry out such monitoring, most Federal reproductive 
effects surveillance studies are carried out by our colleagues at the Centers for 
Disease Control and Prevention. 



QUESTION 4: 

When will EPA's final report on the dioxin reassessment be released? 
ANSWER 4: 

EPA released an external review draft of its reassessment efforts on September 
13, 1994. The draft will undergo a 120-day public comment period followed by 
review by the Agency's Science Advisory Board (SAB). Revisions will be made to the 
document based on these review comments, and a final report is expected to be 
released by Fall, 1995. 



QUESTION 5: 

If a veteran is concerned that his or her future children may have birth defects 
or serious illnesses because of the veteran's toxic exposures, how can he or she get 
accurate information to answer those concerns? Who could they contact at your 
agency for such information? 

ANSWER 5: 

As a public health professional, I always suggest that individuals consult with 
their physicians regarding their concerns about potentially toxic exposures. In 
addition, their physician, or they personally, can contact EPA's Office of Health and 
Environmental Assessment (OHEA) regarding assessments of potential health impacts 
that have been carried out by EPA's scientific programs. For this type of information 
call or fax a request to Dr. William H. Farland, OHEA, USEPA at 202-260-7315 
(phone) or 202-260-0393 (fax). 



410 



GAO 



United States 

General Accounting Office 

Washington, D.C. 20548 



Metliodology Division 



September 2, 1994 

The Honorable John D. RocKefeller IV 
Chairman, Committee on Veterans' Affairs 
United States Senate 

Dear Mr. Chairman: 

We appreciate your additional interest in our work regarding 
veterans of the Persian Gulf war who may be suffering 
reproductive problems resulting from their service in the 
gulf region. In your letter of August 17, 1994, concerning 
our recent testimony entitled Operation Desert Storm: 
ppteptjal for Repro<iu(;tive DysfungtJQn Us Not; Bgin9 
^(jeqMately Monitored (GAO/T-PEMD-94-31) , you asked us six 
questions: 

(1) In the 3 years since the gulf war, has any government 
agency conducted a definitive study to determine whether 
gulf war veterans are experiencing reproductive 
problems? 

(2) Which potentially hazardous substances were brought to 
the gulf by the U.S. military? 

(3) Did DOD have any effective safety precautions in place 
for any toxins? 

(4) What kinds of warning should U.S. troops be given about 
using common toxins (such as pesticides or insect 
repellents) safely? 

(5) What additional questions addressing reproductive 
dysfunction should VA add to its current Persian Gulf 
War Health Registry questionnaire? 

(6) Was GAO able to determine if military personnel are 
possibly exposed to reproductive hazards during routine 
military training? 

In response to your first question, we are not aware of any 
study by VA, DOD, EPA, or any other government agency that 
we believe could properly be characterized as definitive on 
the question of the reproductive outcomes of Gulf war 
veterans. As we stated in our recent testimony and our 
report Operation Desert Stofm: Questions I^emaip on posgjble 



411 



Exposure to Reproductive Toxicants (GAO/PEMO-94-30) , we 
found several major shortconings involving both ongoing and 
planned study efforts conducted or to be conducted by DOD 
and VA. A major study to be conducted by DOD will cover a 
large number of active duty personnel but not reservists. 
Also, the study will not cover certain areas of reproductive 
dysfunction such as infertility. This study will not be 
finished for 3 years. Thus, there will remain no clear 
determination of the existence of certain forms of 
reproductive dysfunction for even more years to come and for 
other issues, such as infertility and for the reservist 
population, there will be no definitive answer even then. 

With regard to your second question, we reported in 
Operation Desert Storm (GAO/PEMD-94-30) that service members 
were exposed to several pesticides and insect repellents in 
the gulf that DOD brought to the region. The decontami- 
nating agent DS2 — containing reproductive toxicants — was 
also brought to the region by DOD. Moreover, the presence 
of other toxic — but not necessarily with reproductive 
effects — agents that DOD brought to the gulf have been noted 
by others. These include various toxicants in petroleum 
products, toxic paints, depleted uranium, chemoprophy lactic 
agents, and the potential toxic effects of combinations of 
these substances with other substances DOD did not bring to 
the region. 

Answering your third question, the scope of our work did not 
allow us to examine safety precautions on other toxicants 
that were not considered to be possible reproductive 
toxicants, and for that reason we did not examine the 
efficacy of these efforts by DOD. However, as you know, we 
did look into educational and protective measures taken 
during the Persian Gulf deployment on the issue of the 
reproductive toxicants we did identify. At this time, it is 
impossible to determine whether or not protection from 
reproductive toxicants was effective for the simple reason 
that it remains undetermined whether or not reproductive 
dysfunction exists, based on the presence of veterans in the 
region. 

With regard to your fourth question, we recommended in our 
report and testimony that DOD develop procedures to better 
ensure that troops are informed of possible reproductive 
toxicants before future deployments. To effect this 
recommendation, we believe it would be constructive to 
convene a panel of experts (such as those at your August 5, 
1994, oversight hearing and other experts in reproductive 
toxicology) , along with relevant individuals from EPA and 
DOD to review current procedures and to make recommenda- 
tions. This might yield the broadest possible information 
on warnings and training requirements that could be 



412 



specifically suited for military exigencies. Additionally, 
we are aware that the Office of Pesticide Programs at EPA 
has worked with DOD to establish directions on the proper 
usage of certain repellents for military purposes (for 
example, insect/arthropod repellent, a protective treatment 
for military battle-dress uniform and uniform fabric) . 
Given the concerns that have been raised about the possible 
role of pesticides in what is known as Gulf War syndrome, it 
may be useful for a panel of experts, such as that suggested 
above, to review the work of the Office of Pesticide 
Programs . 

In response to your fifth question, we believe the most 
important issue concerning the VA Persian Gulf War Health 
Registry — and DOD's registry — is to collect the approved, 
expanded data on infertility and miscarriages for the more 
than 20,000 Persian Gulf veterans who were queried with the 
original code sheet that asked only whether the service 
member had a child with a birth defect and whether that 
child was conceived prior to or after the Persian Gulf war. 
Further, we believe it would be helpful to enlist the 
advice of the expert panel — suggested above — to review 
the completeness of the expanded VA and DOD registry 
questionnaire and to consider the importance and feasibility 
of collecting data on reproductive issues still not covered 
by it. 

With regard to your sixth question, our study did not focus 
on whether military personnel are exposed to reproductive 
hazards during their routine military training. However, 
we are aware that pesticides are commonly used around^ 
encampments during training, that exposure to petroleiim 
products and byproducts is typical, and that exposure to the 
various reproductive hazards identified in the health hazard 
assessment process of the various military services must, by 
necessity occur, albeit in presumably controlled circum- 
stances. In our study, we did not examine the extent or 
duration of exposure to these or other possible reproductive 
toxicants. 

If you have any additional questions regarding our testimony 
or report, please call me on 202-512-3092. 

Sincerely yours. 



^ 



1 { 



Kwai-Cheung Chan 
Director of Program Evaluation 
in Physical Systems Areas 



413 



WRITTEN QUESTIONS FROM CHAIRMAN ROCKEFELLER TO DR. 
SILBERGELD AND THE RESPONSES 



September 7, 1994 

Honorable John D Rockefeller 
Chair, US Senate Committee on 

Veterans' Affairs 
Washington DC 20510 

Dear Sen. Rockefeller: 

I submit this material in response to your questions sent to me in 
writing on August 17, 1994, as follovmp to the August 5th hearing 
on reproductive hazards and military service. As my secretary Ms 
Rhonda Brown explained, I have been away at meetings and on 
vacation until this week, so that my response has been delayed. I 
hope this material is still in time for the record. 

It was truly a privilege to have been part of these hearings . The 
testimony by veterans and, their families was extraordinarily 
eloquent, and for me provided a powerful reminder of why all our 
work is important. Thank you for allowing me to take part in the 
hearings . 

1 . Can chemicals or other toxins cause genetic defects that cause 
birth defects? 

The short answer to this question is, yes. Chemicals and 
other toxic materials (such as radiation) can cause birth defects 
through at least three mechanisms: by damaging genetic material; 
by inducing toxic effects in the developing embryo and fetus,- and 
by affecting the availability of essential nutrients during 
intrauterine development. An example of the first type of 
teratogen (agent that induces a birth defect) is: ionizing 
radiation; an example of the second type is methyl mercury; and 
example of the third type is (possibly) lead competing with calcium 
during intrauterine skeletal growth. 

These are effects that occur as a consequence of exposure of 
the mother, during pregnancy. It is also possible for chemicals or 
other toxins to affect reproduction and development as a 
consequence of exposures prior to pregnancy, in women, and as a 
consequence of exposures of the father. As an example of the 
former (preconception exposures of women affecting their children) 
there is a substantial database on the adverse effects of PCB 
exposures observed in infants and children (see studies by Rogan 
and coworkers on the "YuCheng" cohort of women exposed to PCBs in 
contaminated cooking oil) . As an example of the latter, exposures 
of men to antineoplastic drugs, such as cyclophosphamide, increases 
risks of miscarriage in their partners. Some epidemiological and 
experimental data also indicate that paternal exposures to lead are 



83-529 95-14 



414 



associated with developmental deficits in children. 

In considering this issue, it is important to keep in mind 
that not all birth defects result from genetic damage. Prenatal 
exposures to toxic chemicals can also cause developmental damage by 
inducing alterations in biochemistry of germ cells (eggs and sperm) 
or in the functions of embryonic and fetal organ systems. 

2. You testified at the hearing that men who are exposed to 
demgerous substances might possibly f{>ther children with 
developmental problems. Would these men necessarily show any other 
health problem? If not, is there some type of testing which should 
be done to determine if chemical substances are present in semen or 
if sperm have been damaged? 

These are very complex questions, and our knowledge is still 
very inadequate in many areas related to the paternal contribution 
to development. It is impossible to give general answers to these 
questions, so these comments are based upon specific substances and 
types of effects. Using as an example the toxic metal lead, for 
which there is evidence that paternal exposure may be associated 
with adverse reproductive and developmental outcomes: the effects 
of lead on male reproduction may occur in the absence of readily 
detectable other health problems. This appears to hold true for 
two other male reproductive toxins, dibromochloropropane and the 
glycol ethers. Second, only limited methods are available for 
assessing both exposures and effects of toxic chemicals with 
respect to male reproductive biology. Measuring chemicals in semen 
or ejaculate is useful only for those toxins for which we can 
interpret the results -- for instance, we need to know the 
relationships between exposures and concentrations in this 
compartment . 

While there are a range of sensitive measures of male 
reproductive function available {ranging from counting sperm to 
assessing functional capacity) , we know relatively little about the 
specific effects of toxic chemicals on these parameters. Even for 
a relatively well studied compound like lead, there is still 
uncertainty as to which outcomes -- sperm number, morphology, 
motility, or penetration -- are the most sensitive indicators or 
the best predictors of reproductive dysfunctions. 

3. Are men predisposed to any cancers of the reproductive system 
because of exposure to chemicals or other toxic agents? 

There are some chemicals that have been associated with 
cancers of the male reproductive system. One of the first links 
between occupational exposures and cancer was the famous report by 
Sir Percival Pott on the association between exposures to coal tars 
and scrotal cancer. More recently, two clusters of testicular 
cancer have been reported in workers exposed to f ormamides . 
Concerns have also been raised that socalled xenoestrogens 
(environmental or occupational chemicals that have estrogen-like 
properties) may be increasing the risks of testicular cancer more 



415 



generally in the US population. 

I would like to add to these comments a general recommendation that 
more research is clearly needed in the area of chemical toxicity 
and male reproduction. This is one of the most understudied area 
of toxicology and biology. Congress would do well to specifically 
recommend and fund such institutions as the National Institutes of 
Health, the US Public Health Service, and the EPA to sponsor and 
conduct research in this area. Specific programs such as the 
National Toxicology Program (within the USPHS) should be directed 
to ensure more comprehensive assessment of toxic chemicals to 
include evaluation of endpoints relevant to male reproductive 
risks, within the context of health care reform, it is essential 
to ensure that we collect critical information on the nature and 
extent of reproductive and developmental problems in the US 
population: at present, there is no comprehensive database on 
birth defects comparable to our national cancer surveillance 
systems; little or no information is collected or analyzed on other 
important endpoints such as infertility or rates of miscarriage. 

I hope this information is useful to you. 

Yours sincerely, 



/i^e^c 



Ellen K Silbergeld, PhD' 

Professor of Epidemiology and Preventive Medicine 

and 

Toxicology 

and 

Pharmacology and Experimental Therapeutics 

University of Maryland Medical School 

Baltimore MD 21201 



416 

WRITTEN QUESTIONS FROM CHAIRMAN ROCKEFELLER TO DR. 
PAUL AND THE RESPONSES 

Question 1. You indicated that each woman is bom with all the eggs she is 
ever going to have. Does that mean that a toxic exposure at any point in her 
life could affect her reproductive function for the rest of her life? 

Response. Yes, because a woman cannot replenish her germ cells after birth 
as can the male, a toxic exposure at any point in her life could affect her 
reproductive function by reducing her fertility or the length of her reproductive 
life. At the time of birth, women have about 2 million germ cells in the 
ovaries, and this number is gradually diminished through a natural process of 
destruction called atresia, as well as through ovulation. When the germ cells are 
nearly depleted, a woman undergoes menopause. Theorectically, toxic agents 
could decrease the size of the germ cell pool by killing germ cells or by 
accelerating the natural process of atresia. For example, cancer patients who 
undergo high-dose radiation exposures to the pelvis or treatment with 
chemotherapeutic drugs may be rendered infertile or experience early 
menopause due to killing of the germ cells. Studies have also shown that 
women who smoke cigarettes undergo earlier menopause than women who 
don't smoke; animal investigations suggest this effect may be due to an 
acceleration of the natural process of germ cell atresia. 

However, there are a number of important points to consider about the 
effects of toxic agents on female reproduction. First, the size of the female 
germ cell pool at birth is large, so that some destruction could undoubtedly be 
tolerated without producing adverse effects on reproduction. Second, the adult 
ovary contains germ cells in different stages of growth: the vast majority are 
small, resting germ cells; others are undergoing partial growth followed by 
atresia; and one egg per month is selected to progress to complete maturation 
and ovulation. The clinical effects of exposure will depend in part on which of 
these germ cells is targeted by the toxic agent. Finally, reproductive effects 
from toxic exposures are also influenced by the age at which exposure occurs. 
For example, the same dose of radiation may cause sterility in a woman in her 
40's, while it causes only temporary menstrual disturbances in a younger 
woman. This is because, due to atresia, the size of the germ cell pool is much 
smaller in the older woman than in the younger woman. 

In general, we know very little about the effects of specific occupational or 
environmental exposures on female reproduction, and this area should be an 
important research priority. 

Question 2. On our first panel at the hearing, we heard about extreme pain 
experienced by wives of many Gulf War veterans during sexual relations with 
their husbands. What could be causing the kinds of problems they describe, and 
what kinds of testing should be done? 

Response. To my knowledge, pain on intercourse has never before been 
reported in relation to a toxic environmental exposure. Therefore, I can only 
conjecture about possible causes of these effects based on my general 
experience as a gynecologist. As 1 understand it, the pain described by the 
wives of the veterans is vaginal pain that occurs on contact with their 
husbands' semen. 

First, this type of pain on intercourse could be due to vaginal infections. 
Some vaginal infections are due to sexually transmitted agents (e.g.. 



417 

trichomonas), while others (e.g., yeast infections) are usually due to alterations 
in the normal milieu of the vagina that favor the overgrowth of the offending 
agent. For example, women who are diabetic or who take antibiotics are prone 
to yeast infections for this reason. Also, women whose immune systems are 
suppressed (e.g. women infected with HIV) may have chronic yeast infections. 
It may be that, for some reason, the wives of the veterans have chronic vaginal 
infections. This hypothesis could be easily tested by examining the affected 
women and by testing their vaginal secretions for infectious agents through the 
use of wet mounts (examination of the secretions mixed with a few drops of 
saline or potassium hydroxide under a microscope) and/or cultures. 

Secondly, the pain could possibly be due to an irritant or allergic skin 
reaction that occurs upon contact with some agent in the semen. In my 
gynecology practice, 1 have occasionally seen women who experience vaginal 
irritation and pain on contact with their partners' semen; the symptoms 
subsided with use of condoms. 1 have also seen women who develop vaginal 
irritation and pain when they use contraceptive foams or jellies or deodorized 
douches. In these cases, the reaction may be due to chemicals contained in 
these products. 

In view of this clinical experience, the question arises as to whether there 
might be some agent in the semen of the veterans that is causing an irritant or 
allergic contact dermatitis in their wives. The first step one could take to test 
this hypothesis is to examine the women shortly after intercourse when they are 
experiencing symptoms. One would expect to see vaginal redness and irritation. 
I would also advise temporary use of condoms to see if avoiding contact with 
semen resolves the problem. If these simple tests suggest that an irritant or 
allergic response might be occurring, the next logical and most difficult step 
would be to determine what agent(s) are responsible for the reactions. The type 
of tests that might be useful here are beyond my area of expertise. Allergy 
testing might be appropriate, as well as the use of assays to measure toxic 
agents in semen. However, given the large number of agents to which the 
Persian Gulf War veterans were exposed, it would be inordinately expensive 
and impractical to test for all possible agents. One would have to develop some 
rational plan for selecting certain agents for testing based, for instance, on their 
ability to persist in the body long after exposure, to concentrate in semen, and 
to cause irritant or sensitization reactions. This information may not be 
available for many of the agents to which the veterans were exposed. 

Finally, vaginal pain during intercourse can be due to other factors such as 
vaginal dryness. Decreased estrogen (e.g. in menopausal women) can lead to 
thinning of the vaginal tissues and dryness, but should be accompanied by 
menstrual changes. It is also possible that stress can interfere with vaginal 
lubrication during intercourse. While it less likely that these factors account for 
the symptoms as described by the veterans' wives, it is important to consider 
all possible etiologies in attempting to explain these problems. 

Question 3. What suggestions would you offer to VA to make sure that they 
gather the information necessary to warn veterans about possible reproductive 
problems, including the risks of birth defects? 

Response. Under the federal Hazard Communication Standard, workers in 
the United States are afforded the "right to know" about the potential health 
hazards associated with chemicals that they use on the job. Under this 
Standard, employers have a duty to warn workers of potential hazards through 



418 

pre-placement and periodic training programs and through provision of Material 
Safety Data Sheets which contain information about hazardous chemicals. Part 
of the training includes informing workers about ways to protect themselves 
from exposure to these toxic chemicals. 

In my opinion, military personnel should be afforded similar rights, and 
adequate warnings and protective advice should be given before deployment in 
high-risk settings. This would require that experimental animal and human data 
on potential exposures be thoroughly evaluated by appropriate agencies and that 
the information be shared with military personnel in a way that is practical and 
understandable. 

In the case of veterans, deleterious exposures may have already occurred and 
the question becomes how to inform them of potential adverse health effects 
of those exposures, including reproductive effects. If it has not already been 
done, I would suggest that the VA review existing data (experimental animal 
and human) on the reproductive and developmental effects of all agents 
relevant to the veterans. This information can be summarized and shared with 
veterans through a number of avenues including, for example, fact sheets, 
telephone hotlines, or through in-person consultations with VA health 
personnel. Since many agents have not been well evaluated for reproductive 
effects, it would be important as part of this education process to let veterans 
know when information about an agent is lacking or when that information is 
uncertain because it is based on limited animal data. As I indicated in my 
testimony, it is also important that the VA support well-conducted research to 
fill in the data gaps where they exist. 



WRITTEN QUESTIONS FROM CHAIRMAN ROCKEFELLER TO DR. 

MATHER (DEPARTMENT OF VETERANS AFFAIRS) AND THE 

RESPONSES 

Question 1. You stated in your testimony that in the 1984 HHS study 
conducted by CDC on birth defects, there was no difference in birth defects 
among fathers who served in Vietnam and fathers who were not Vietnam 
veterans. It is my understanding that the 1984 study did show an increased risk 
for spina bifida, cleft lip, and cleft palate, and some tumors and cysts in 
children fathered by Vietnam veterans who were exposed to Agent Orange. Is 
that correct? 

Response. The CDC Birth Defects Study did not find an association between 
Vietnam veteran status and major birth defects (all types combined). Thus 
Vietnam veterans, in general, did not have an increased risk of fathering 
children with birth defects. The study also used a subjective score of possible 
Agent Orange exposure, the Exposure Opportunity Index (EOI). The EOI was 
based on the veteran's military occupation, location, and time of service in 
Vietnam. There were two methods for estimating agent orange exposure 
(Exposure Opportunity Index). One method was based on an evaluation by 
service specialists, the other method was based on the veteran's self-report. 
(Birth defects were categorized into 96 groups for the purpose of analysis. The 
risk for fathering children with spina bifida, cleft lip with or without cleft 
palate, and "other neoplasms" was found to be higher for Vietnam veterans 
with higher EOI scores. The increased risk of spina bifida was associated with 
higher EOI scores as measured by both methods. Increased risk of cleft palate 



419 

and other neoplasms were only associated with the self-reported EOI measure. 
The authors correctly point out that due to the multiple hypotheses being tested 
in this study, some statistically significant differences were to be expected, 
even if no true differences in risk existed in the Vietnam veterans and the 
controls. A statistical difference does not necessarily mean that there are true 
differences in the risk of adverse reproductive outcomes. In analyzing this, and 
other, studies of reproductive health in Vietnam veterans, the National 
Academy of Sciences (NAS) concluded that there was insufficient evidence of 
an association of Vietnam service and an increased risk of birth defects. 

Question 2. It is my understanding that at a recent teleconference. Dr. 
Frances Murphy suggested there was no reason for Persian Gulf veterans to 
postpone having children. On what information does she base this 
recommendation? 

Response. On July 21, 1994, VA broadcast a satellite video teleconference 
updating VA health care providers, administrators, and veterans representatives 
on Persian Gulf experience and health. The focus of the conference was a 
summary of the findings and recommendations of the NIH Persian Gulf 
Workshop, and VA's response to the recommendations on post-traumatic stress 
and development of a uniform case assessment protocol for unexplained 
illnesses of Persian Gulf veterans. In response to a question from the audience. 
Dr. Murphy stated that though many Persian Gulf veterans are particularly 
concerned about reproductive health problems including birth defects, at present 
scientific information did not support a recommendation to delay conception 
and child-bearing. This recommendation is based on the information obtained 
from the CDC, the Mississippi State Health Department, and the Jackson VA 
Medical Center on the children in two Mississippi National Guard Units and 
the Persian Gulf Registry. These sources of information do not provide 
conclusive epidemiologic information concerning risk of adverse reproductive 
outcomes in Persian Gulf veterans; however, both fail to identify an increased 
risk of birth defects in association with Persian Gulf service. It would be 
imprudent to base a recommendation concerning delay in childbearing on 
anecdotal information. VA will support and expedite efforts to obtain more 
complete information on the reproductive health of Persian Gulf veterans. 

Question 3. During the hearing, we heard some very compelling testimony 
about the sexual problems that Gulf War servicemen and their wives are 
having. These problems seem to be related to something in the veterans' 
semen, which may even be causing birth defects. According to scientists, the 
semen should be tested for pesticides, heavy metals, or other abnormalities. 
And yet, one of our witnesses, Kelli Albuck, told us that the military hospitals 
refuse to do the necessary tests to find out what's wrong. Since our hearing, 
what efforts have you made to ensure that VA will do this testing? 

Response. Several Gulf War veterans have reported that their wives 
experience burning on exposure to their semen. To our knowledge, pesticide 
levels and heavy metal determinations in semen are not available for standard 
clinical testing. 

These may be fruitful areas to explore in case-control research studies in the 
near future. As the non-governmental scientific experts pointed out at the 
hearing, little is known about the male reproductive toxicity. VA is committed 
to explore these important scientific questions with the input of both federal 
and non-federal experts. 



420 

Question 4. The VA recently announced a proposal to conduct an 
epidemiological study of 1 0,000 veterans and active duty members who served 
in the Persian Gulf. Will information such as reproductive problems, birth 
defects, and children's illnesses be obtained in this survey? How will this study 
be coordinated with the recommendations of the National Academy of 
Sciences' Medical Follow-up Agency? 

Response. VA is planning a national survey of a representative sample of 
Persian Gulf veterans and a comparison group of Gulf era veterans who were 
not deployed to Southwest Asia. The purpose of this epidemiologic study is to 
determine the prevalence of symptoms and adverse reproductive outcomes in 
veterans and their family members. VA, DOD and HHS are working 
cooperatively on questionnaire development. The staff of the National Academy 
of Sciences have been briefed on the proposed survey and will be updated as 
planning progresses. VA has sought the advice of NAS on Persian Gulf health 
concerns. Available NAS recommendations will be incorporated into the survey 
design. 

Question 5. Has VA ever studied the incidence of birth defects in children 
bom to atomic veterans, Vietnam veterans, or Persian Gulf veterans? 

Response. VA has participated in or supported research on reproductive 
problems in Vietnam veterans and Persian Gulf veterans. We are not aware of 
any research conducted on atomic veterans which VA conducted. 

Question 6. Do you have any plans to conduct research on any reproductive 
problems for atomic veterans, Vietnam veterans, or Persian Gulf War veterans? 

Response. VA plans to conduct a study of Vietnam Women Veterans which 
will focus on reproductive problems and cancers. In addition, VA has a 
contract with NAS for an ongoing review of the scientific literature including 
studies of reproductive outcomes. Future VA investigations of reproductive 
problems for Persian Gulf veterans includes epidemiologic studies such as the 
National Survey of Persian Gulf Veterans, and participation in the U.S. Navy 
epidemiologic study on birth outcomes of Gulf War veterans. VA and DOD 
have jointly contracted with the National Academy of Sciences to study the 
health of Persian Gulf veterans. 

NAS recommendations for future research will be considered, including 
those on reproductive problems. 

Question 7. In their report, GAO pointed out that the first 20,000 veterans 
enrolled in the Gulf War registry were not asked about infertility and 
miscarriage. Don't you think these veterans should be contacted so that 
information can be included? 

Response. The original VA Persian Gulf Registry included questions on birth 
defects but did not address other aspects of reproductive health. The Registry 
has been revised to include questions on infertility, miscarriages, still births, 
neonatal deaths, and infant deaths. Secretary Brown has asked that VA staff 
provide guidance on the optimal method to obtain information on the 
prevalence of these conditions in Persian Gulf veterans. Serious consideration 
is being given to this matter and recommendations will be made to the 
Secretary and Under Secretary for Health in the near future. 

Question 8. Most veterans in the Persian Gulf War registry have medical 
problems. If a healthy PGW veteran experiences a miscarriage or stillbirth, or 



421 

has a child with birth defects or who dies during infancy, is that information 
included in a PGW registry? 

Response. The VA Persian Gulf Registry is a health registry program which 
provides a medical history, physical examination and screening laboratory 
testing for veterans and military members who served in the Persian Gulf VA 
strongly encourages veterans who are asymptomatic but who have concerns or 
questions about the health consequences of service in Southwest Asia, as well 
as those Gulf War veterans who are experiencing health problems, to 
participate in the Persian Gulf Registry program. The medical history on the 
revised Registry questionnaire asks each participant about the occurrence of 
birth defects, miscarriages, stillbirths, neonatal deaths, infant deaths and 
infertility after the Persian Gulf War. This information will be recorded on 
veterans who participate in the Registry examination program irrespective of 
their general health status. 

Question 9. Please explain how VA tracks the incidence and prevalence of 
various diseases and disorders, such as infertility or birth defects. When 
increases are identified, how does this information get used, so that veterans 
who were harmed become eligible for compensation, or future military 
personnel can be protected from similar hazardous exposures? 

Response. Incidence and prevalence of various diseases and disorders are 
estimated using focused epidemiologic research studies. The results of such 
studies can be used as the basis for protection of ftiture military personnel or 
development of compensation programs for affected veterans. There is no 
ongoing health surveillance database which tracks reproductive health of 
veterans. 

Question 10. What do you think VA can do to help civilians who might 
have been harmed by their spouses' military service? 

Response. VA is deeply concerned about the possibility that families might 
have been harmed by their spouses' military service. We are committed to 
investigate this possibility through scientific research studies. We will use 
outreach programs to provide veterans and their families with updated 
information on these investigations and the current state of knowledge 
regarding such issues. VA was given special authority to provide readjustment 
and family counseling to families of Persian Gulf veterans and has done so 
through its Family Support Program. VA and DOD are also coordinating efforts 
to provide medical evaluations of unexplained illnesses after Persian Gulf 
service. VA will utilize its ftill legal authority, now and in the ftiture, to 
provide care for veterans who have served their country. 

Question 11. One way that VA could be helpful would be by informing 
veterans that particular past exposures could cause future reproductive 
problems. This might influence veterans' decisions on whether to have children, 
especially if they have already had multiple problems like those described by 
our panel of veterans at the hearing. How do you propose that VA could be 
more helpful in terms of conducting studies and disseminating information? 

Response. One of the inherent difficulties VA has faced in providing 
information to veterans concerning future reproductive problems associated 
with exposures encountered while serving in the military is that, in the past, 
exposure information provided to the VA was limited. Furthermore, in cases 
where an exposure is known to have occurred, the body of scientific knowledge 



422 

concerning the risk of adverse reproductive outcomes is often not adequate to 
provide sound recommendations regarding childbearing. VA will explore ways 
to promote research in this area in the future. 

VA is involved in several activities which may prove helpful for the future. 
VA has been asked to assist DOD in planning medical surveillance for 
deployment of military members. Medical hazards and risks are being assessed 
in the pre-deployment, deployment and post-deployment phases of military 
actions with attention to monitoring, prevention and surveillance for the health 
consequences of hazardous exposures. 

Information obtained from VA and non-VA research efforts can be 
disseminated to interested veterans through newsletters, briefs, media coverage, 
and veterans service organization publications. An important aspect of 
information dissemination involves education of VA, military and non-federal 
physicians about reproductive toxicity as it relates to veteran populations. This 
can be accomplished through national medical meetings, scientific publications 
and continuing medical education sessions. 

Question 12. Did the Atomic Medicine Division, which was classified in the 
1940s, have any information which would be helpflil in determining if radiation 
caused reproductive dysfunction, cancer, or birth defects in children? 

Response. Relatively little information exists on the past activities of the 
Atomic Medicine Division. A recent review of some archived records have 
revealed minutes of a meeting regarding planning of civil defense functions. No 
records on the Atomic Medicine Division have been uncovered which relate to 
reproductive dysfunction, cancer or birth defects in children. 

Question 13. An upcoming report by EPA will apparently conclude that 
dioxin can cause infertility and reproductive problems in men. A study by 
another witness at the hearing, Linda Schwartz, seems to provide preliminary 
evidence of a similar effect on women Vietnam veterans. How will the EPA 
report affect medical care and compensation for Vietnam veterans who were 
exposed to Agent Orange? 

Response. We cannot comment on the EPA chapter on Risk Characterization 
of dioxin since it is available only as a preliminary draft. The potential for 
dioxins to cause reproductive toxicity in animals has been recognized for many 
years. However, a wide variability of responses exist across species and the 
significance of this data to human populations is the subject of much scientific 
controversy. 

The National Academy of Sciences (NAS) will provide VA an updated 
review of the available scientific literature on dioxin and related compounds. 
We expect that review to be completed in late 1995. Based on the 
recommendations of the NAS committee, VA will reassess its medical care and 
compensation programs for veterans at that time. 

Question 14. What will VA do to follow up on the study of women 
veterans? 

Response. VA Environmental Epidemiology Service is planning a study of 
Women Vietnam Veterans Reproductive Health. A preliminary pilot 
investigation is underway and the study protocol is being prepared for peer- 
review. The formal study is planned for FY 1996. 



423 

Question 15. According to information VA provided the Committee, an 
unusually high number of young Gulf War veterans have been diagnosed with 
testicular cancer. Similar problems have been found in a small study involving 
Vietnam veterans living in West Virginia and a Department of Health and 
Human Services study of dogs that were used by U.S. troops in Vietnam. What 
is VA planning to do to follow up on these findings? 

Response. The VA Persian Gulf Registry provides a mechanism for 
monitoring health trends and developing hypotheses for further investigation in 
this self-selected population of Persian Gulf veterans. The primary purpose of 
the Registry program is provision of medical care; it should not be viewed as 
an epidemiologic or research instrument. Testicular cancer is a common cancer 
in males of military age. It is not possible to tell from existing information 
whether the incidence of testicular cancer is unusually high because the VA 
Registry does not provide a means to determine incidence or prevalence of 
conditions such as testicular cancers, nor does it include a control population 
for comparison. 

VA is planning several epidemiologic studies of Persian Gulf veterans which 
may help clarify the questions raised by the Committee concerning testicular 
cancers. VA will carry out a National Persian Gulf Survey and will participate 
in the U.S. Navy epidemiologic study of Persian Gulf veterans. The 
Environmental Epidemiology Service has recently completed and published a 
case-control study which did not show an association between potential for 
Agent Orange exposure and increased risk of testicular cancer in Vietnam 
veterans. VA has contracted with NAS for a literature review on the health 
effects of herbicides used in Vietnam and also for a study of the health effects 
of Persian Gulf service. Future studies and research efforts will be coordinated 
based on NAS recommendations. A preliminary report is expected in late 1 994. 



APPENDIX 5.-EPA DIOXIN REASSESSMENT AND 
ARTICLES REGARDING REPRODUCTIVE HAZARDS 



Unitsd Statss Communications. Education. Saplamtxr 

Environmental Protection And Public Attain 

Agancy (1700) 



oER^ 



STATEMENT OF LYNN GOLDMAN, M.D. 

ASSISTANT ADMINISTRATOR FOR PREVENTION, 

PESTICIDES, AND TOXICS 

SEPTEMBER 13, 1994 



Today the EPA is releasing a "public review draft" of its dioxin 
reassessment. This release marks a major milestone in our effort to 
reevaluate our scientific understanding of dioxin. More than 100 
EPA and outside scientists have worked for over three years to 
develop the current draft of the reassessment. Over the next 120 
days , the EPA v«ll be taking public comments on the draft document. 
Early in 1995 EPA's Science Advisory Board will conduct a formal 
scientific peer review. We v^ conclude the reassessment about a 
year from now, incorporating appropriate changes that have been 
indicated by the public comments, peer reviewers and the SAB. 

Dioxins are a group of chemical compounds inadvertently 
created through a number of activities including: combvistion, 
certain types of chemical manufacture, chlorine bleaching of pulp 
and paper, and other industrial processes. Dioxin is produced in 
very small quantities compared to other pollutants (around 30 
pounds annually); however, because it is highly toxic, it has been 
treated as a significcuit environmental pollutant since the early 
1970's. EPA first took action against dioxin regarding the herbicide 
2,4,5-T in 1979. Since then, EPA has expanded its dioxin control 
efforts to each of its major programs. 

In 1985 EPA published a scientific review of the health effects of 
2A7,8-TCDD, the most toxic of the dioxin family of compounds. 
That assessment serves as the scientific basis for dioxin risk 
estimates for all EPA programs. Since 1985 a number of scientific 
and newspaper reports have raised questions about the risks posed 
by dioxin. The draft study not only updates the 1985 doctmient, but 
also represents an ongoing process to build a broad scientific 
consensus on dioxin's toxic effects. 



425 



426 



To help foster this consensus, EPA has worked to make each 
phase of the dioxin reassessment an open and participatory process. 
These efforts have included the involvement of outside scientists as 
principal authors of several chapters, several public meetings to take 
comment on our plans and progress, and publication of earlier drafts 
of our work for public comment and review. We cire continuing this 
participatory process by making the current draft available for public 
conunent and full scientific review. When this process is completed, 
we anticipate having an up-to-date and thorough scientific 
assessment of dioxin that is at the cutting edge of envirorunental 
toxicology. 

Regarding health risks, the draft study reaffirms the 
association of dioxin and cancer. In its 1985 assessment, EPA 
concluded that dioxin is a proven animal carcinogen and a probable 
human carcinogen. Today's report reaches the same conclusion, but 
with greater confidence. Based upon both animal and human 
evidence, EPA's estimate of dioxin's cancer potency is essentially 
unchanged from that of 1985. 

The draft reassessment differs significantly from the 1985 
dociunent in its evaluation of dioxin's non-cancer effects. Today we 
have a stronger body of evidence to suggest that at some dose, 
dioxin exposure can result in a number of non-cancer health effects 
in humans. These effects may include developmental and 
reproductive effects, immune suppression, and disruption of 
regulatory hormones. We have no direct evidence to show that any 
of these non-cancer effects occur in humans at everyday levels of 
exposure. However, we can infer from the data that average 
everyday exposures are dose to exposures that are known to cause 
such effects in laboratory animals. 

The draft study also identifies dioxin sources that are known to 
contribute to environmental contamination. Waste combusfion 
accounts for about 95% of all the known emissions, with medical and 
murucipal waste combustion dominating the combustion sources. It 
is likely that there are a number of unidentified sources of dioxin in 
the U.S. and that we do not have sufficient information about 
enussions from known sources to provide precise estimates. It is also 



427 



possible that much of the dioxin that contributes to human exposure 
results from past dioxin emissions recirculating in the environment. 
Although there are some natural sources of dioxin, such as forest 
fires, it seeir\s clear that dioxins are primarily a product of modem 
industrial society. 

We believe that the pathway for exposure to humans is 
primarily via airborne dioxins that settle on plants, and that are 
passed on through the food chain and associated particularly eith 
fat. The federal government emphasizes that the benefits from a 
balanced diet far outweigh any theoretical risks from dioxin 
exposure. 

While the reassessment has been underway, EPA has continued 
to move forward in implementing its dioxin control programs. EPA 
has taken action imder every one of its major statutes to control the 
risks of dioxin, and we believe these activities have made, and will 
continue to make, major strides in reducing dioxin emissions. Recent 
actior\s taken by EPA include proposing air emission standards for 
municipal waste incinerators, proposing stringent water effluent 
standards for pulp and paper mills and waste incinerators. No later 
than next February, EPA will propose strict air standards for 
reducing dioxin and other emissions from medical waste 
incinerators. 

While the science of the reassessment is undergoing peer 
review, EPA will be examining the reassessment's policy implications 
to determine what changes, if any, are needed in existing programs. 
I want to stress that existing EPA efforts and programs will not be 
changed on the basis of this draft reassessment,however, they may 
change sigiuficantly after the completion of the peer review. EPA is 
committed to developing an agency-wide strategy for managing 
dioxin risks, concurrent with completion of the dioxin reassessment. 
As with the reassessment, we want to provide an opportunity for 
early public input into our policy evaluations. This spring, EPA Vkdll 
hold dioxin policy workshops to explore the policy implications of the 
reassessment. The details of these workshops v«ll be aimounced 
later. 



428 



This massive scientific effort has made it dear that there are 
significsmt data gaps that are critical to our imderstanding and 
effective management of dioxin. As a consequence, EPA has begim a 
major initiative to expand the understanding of dioxin sources, 
environmental pathways and human exposure. Oiu' highest priority 
will be to identify additional data to improve the reassessment; 
however, the exposure initiative will extend beyond the 
reassessment into future years. 

As a peirt of this effort, today we are railing on all peirties to 
voluntarily submit any data that can help us better understand dioxin 
exposure. The EPA is requesting that industry, public interest 
groups, state and local governments, academia, and hospital 
facilities examine their files for existing data. We need information 
on dioxin sources, releases and levels in air, water, soU, food, animal 
feed, and human tissues. In addition to this voluntary call-in of 
existing data, EPA is calling on industries that are potential dioxin 
soxirces to volvmtarily work with the Agency to devise emd implement 
emissions testing programs. 

The reassessment represents a major expansion of EPA's 
scientific imderstanding compared to our previous assessments of 
dioxin toxicology. Because many of the studies included in the 
reassessment have only recently been part of the scientific literature 
and our integration of this evidence is entirely new, it is important 
that the reassessment undergo thorough public and scientific peer 
review. At the same time, because the general thrust of the 
reassessment is consistent with our past scientific basis, we feel 
confident in aggressively pxirsuing our ongoing dioxin control 
efforts. This report, once it has completed peer review sometime 
next year, will give us the best scientific basis possible to gxiide our 
continuing efforts to curb dioxin risks. 



429 



Dioxin and Its Effects 
on Reproductive Systems 

Claude Hughes, Ph.D., M.D.* 



Reproductive and developmental toxicology refers 
to the effects of exposure to particular com- 
^ pounds on many aspects of reproductive function 
and development. Toxic outcomes include disruption 
in male or female animals of normal processes that 
are known to be essential for reproduction and detri- 
mental effects on the developing fetus that may 
appear at birth or much later in life. These detrimen- 
tal effects include malformations and abnormal func- 
tion of organ systems, such as alterations in learning 
and other behaviors, including sex-appropriate 
behaviors. 

In the Environmental Protection Agency's (EPA) 
reassessment of dioxin conducted as open public 
meetings in September 1992, the injurious effects of 
dioxin on reproduction and development were ana- 
lyzed. Various human and animal studies of the 
reproductive or developmental effects of dioxin were 
evaluated. In addition, the levels of dioxin that had 
effects on reproduction and development were com- 
pared to the amounts of dioxin and related chemicals 
that we currently bear. 

The people of Maine face a real health concern 



1051-2438/ 1993/0303J)n:S03aO'0 

© 1993 BMI Publishing Group 

' CH IS Associate Proressof or Obstetrics 

University School ot Medicine Address cot 

requests to Claude Hughes. Ph D . M D . Duke 

PO Box 3418, Durham. NC :mo 

This article is adapted irom testimonv given betore the Maine 

Department oi Environmental Protection Public Hearing re Proposed 

Chapter 534 Surlace Waters Toxics Control Program Intenm Statewide 

Cntenon tor Dioxin; Augusta. .Vlaine: .\ovember n. '.**2. 



nd Cvnecology, Duke 
•spondence and repnnt 
nivesitv Medical Center, 



regarding current exposure, current body burdens, 
and current intake of dioxm and related compounds. 
The intake of contaminated fish would incrementally 
add to that exposure and those hazards. 

There currently exist several reliable studies [1-81 
that demonstrate reproductive and developmental 
effects from dioxin in animals and people at relatively 
low levels of exposure. The levels of dioxin that can 
be realistically expected to occur in people in .Maine 
now and the levels in these studies are similar. Thus it 
is reasonable to be concerned that the effects reported 
in these studies may occur in similarly exposed popu- 
lations in Maine. 

In 1990, when EPA decided to approve state dioxin 
water quality standards up to 1.2 parts per quad- 
rillion ippq), the Agency still was not focusmg on 
reproductive, developmental, and other noncancer 
effects of dioxin. Researchers at EPA, National 
Institute of Environmental Health Science (NIEHS), 
and universities, however, had concerns and had 
been actively investigating these kinds of effects from 
the 1970s to present. EPA's current attention to these 
noncancer end proints has been exemplified by a num- 
ber of activities, including dedication of an entire 
half-day at the EPA's reassessment of dioxin to repro- 
ductive and developmental effects and immunotoxici- 
ty effects of dioxin as well as updating developmental 
toxicity guidelines and publishing them in the Federal 
Register m 1991. 

The effects of dioxin toxicity on reproduction and 
development may be more important than carcino- 
genesis because when one talks about effects on the 



430 



developing brain one is talking about the functional 
competency of tfie next generation. Developmental 
biology issues are framed differently than carcinogen- 
esis issues. During the development of the brain or 
other organ systems, the window in time during 
which critical events occur is in fact usually quite lim- 
ited. Narrow time-limited exposures may have pro- 
found effects in terms of disrupting normal organiza- 
tion of tissues or systems within the body. Exposure 
to dioxin or other agents can have an important effect 
over a short period of time. Thus, an exposure in 
early or midpregnancy can indeed be transient for the 
adult mother but have permanent effects on the off- 
spring. 

This approach to the effects of toxic exposure is dif- 
ferent from our thinking about cancer as the end 
point. With regard to cancer, it may take years of 
ingestion or exposure to elicit a modest increase m 
cancer risk. The developmental effects resulting from 
dioxin exposure are stochastic, rather than probabilis- 
tic. In this regard, the risk from exposure to dioxin is 
expressed in the same way as the risk from exposure 
to radiation. The risk of experiencing developmental 
effects from a given exposure is more homogeneously 
spread out across the population exposed. Everybody 
in the exposure group is assumed to run the same risk 
of experiencmg an effect. 

Scientists do not know at this time whether in addi- 
tion to early exposures in fetal or intrauterine devel- 
opment there are other periods in human life that are 
also exquisitely sensitive to perturbation. The penpu- 
bertal interval is a period that may also prove pivotal 
in terms of susceptibility to toxic exposures. Other 
important unknowns concern the fate of absorbed 
toxins once they are mobilized or metabolized in the 
body. For toxins that accumulate in body fat such as 
dioxin, continued ingestion over time results in an 
age-associated depot of the compound in that tissue. 
During intervals of weight loss when body fat is 
mobilized, dioxin must mobilize as well. The conse- 
quences of shifting this toxicant from fat stores to 
other metabolic compartments in the body are cur- 
rently unknown. Furthermore, 30% to 50% of preg- 
nant women commonly have an interval of anorexia 
early in pregnancy. We do not know how high the 
peak blood levels of dioxin may be when those 
women in the first trimester, especially late in the first 
trimester, mobilize fat stores. There are no data that 
assess the changes in blood levels, or other target tis- 
sue organ levels, when fat mobilization occurs. 

Dioxin and related chemicals exert effects bv bind- 



ing to very specific nuclear receptors called Ah recep- 
tors, which are similar to steroid hormone receptors. 
These receptors are proteins that are located in the 
nucleus of cells, and generally there are 1,000 to 2,000 
per cell. For these types of receptors, if a few hundred 
are occupied, biological effects are elicited. An 
mcreased response occurs with an increasing percent- 
age of receptors occupied. Dioxin works by binding 
to these Ah receptors. At a concentration of 1 ppq, a 
teaspoon of water contains over 1.6 million molecules 
of dioxin. While all 1.6 million molecules of dioxin 
will not end up in one single cell such as a neuron in 
the brain, it is clear that a very dilute solution con- 
tains a large number of dioxin molecules, which are 
more than enough to occupy the active receptors in 
the cells and hence to produce adverse effects. This 
mode of action is very different from that of a com- 
pound like aspirin, which is a fairly general, weak 
inhibitor of a widely dispersed enzyme that involves 
prostaglandin synthesis. Aspinn does not have very 
specific effects, whereas dioxin does. 

The background level in humans for dioxin is 
approximately 1.3 ng/kg, and the sum total of activi- 
ty of all dioxin-like chemicals in humans (known as 
to.xic equivalents) is approximately 7 ng/kg [9-11). 
Keeping these figures in mind, it is instructive to look 
at the studies that have been done in the last 15 years 
that have examined some developmental end points 
and some reproductive effects. 

In a National Institute of Occupational Safety and 
Health (NIOSH) study [7], men who were occupahon- 
ally exposed to dioxin showed suppression of testos- 
terone levels. The body burdens in the men showing 
suppression were in the range of 5 to >19 ng/kg. Even 
allowing for our inability to determme whether current 
body burdens or previous exposures were the mecha- 
nistic cause for these reduced testosterone levels, such 
effects are of concern and are clinically sigmficant. 

Reasonable cnticism of the NIOSH study includes 
noting that it is likely that these men were exposed to 
other chemicals. Although the researchers looked for 
other possible chemical mediators of the observed 
low testosterone levels, they did not find any, and the 
other known chemicals these workers were exposed 
to are not known to affect testosterone levels. 

In a study by Mably and colleagues (3-51, pregnant 
rats were given a single dose of dioxin on day 15 of 
pregnancy. The lowest dose studied was 64 ng/kg, 
compared to background levels in the U.S. population 
of around 7 ng/kg. That expenmental dose did not 
affect birth weights or adult weights of these off- 



1 and lis Ertects on Reproductive Svsiems 



431 



spring. It did, however, alter male fetal development, 
such that these male rats were observed to have com- 
promised sperm production and diminished size and 
weight of other hormone-dependent tissues, such as 
prostate and epididymis. In addition, these males 
exposed to dioxin in utero showed demascuiinization, 
with altered sexual behavior including markedly 
increased mount and intromission latency and 
increased lordosis response after estrogen priming. 
These behavioral changes are a brain effect. When 
studies of similar design usmg other agents have 
shown perturbations m normal sexual behavior, sub- 
sequent studies in every instance have confirmed that 
these observed effects are associated with structural 
or biochemical changes in how the brain functions 
[13,14]. Anatomic and chemical studies of the brains 
of dioxin-exposed rats are underway. 

In a study of monkeys by Bowman and colleagues 
(121, the offspring who were exposed in utero to 22 
ng/kg of dioxin showed specific defects in learning 
ability, with disordered object learning but unim- 
paired spatial learning. In this primate model, this 
behavioral index of learning in the offspring was 
compromised by a dose that is only about three times 
higher than what we humans currently bear as a 
result of environmental exposure.' 

If levels shown to exert adverse effects in animal 
studies are somewhat higher than the current levels 
of dioxin in human populations, then why is there 
concern about human health? In part, the answer is 
that none of these studies identified levels at which 
reproductive or developmental effects did not occur. 
Therefore, we do not know whether the levels that 
exert effects are truly different than the dioxin levels 
we currently bear. At this time there is very little 
information to allow us to establish whether humans 
are more or less sensitive to dioxin than other ani- 
mals, or whether wide differences in sensitivity to the 
effects of dioxin occur within the human population. 

This issue is not clarified in the only epidemiologi- 
cal study available that examines birth defects m a 
human population exposed to dioxin as a result of the 
1976 industrial explosion in Seveso, Italy (15). The 
companson of human and animal data summarized 
here would suggest that humans are much more sen- 
sitive to these effects than are laboratory animals, 
since comparable effects occurred in men at body bur- 
dens of dioxin that were several times lower than m 



The rettabiiity ot this study was questioned at one point; howevef at 
EPA* reassessment ot dioxm in September I'^S. Linda BimtMum . 
.•thers M EPA. '.vho have audited it. report the ^tudv to be reliable 



experimental animals. Given these observations 
where the body burden in human study subjects or 
the animals are only three to nine times greater than 
present human body burdens, it is prudent to con- 
clude that there is little margin of safety between lev- 
els that all of us currently bear and the level of dioxin 
and related compounds shown to produce adverse 
effects on male reproduction and central nervous sys- 
tem development, as manifested in sexual behavior 
and learning. This conclusion was presented at the 
EPA's reassessment of dioxin in September 1992 and 
none of the assembled panel members exptessed dis- 
agreement at that time with these correlations and 
conclusions. The acknowledgment of that conclusion 
by EPA is described in the October 9, 1992, memo that 
Erich W. Bretthauer, Assistant Administrator for 
Research and Development, sent to then EPA 
Administrator William Reilly: 

My interpretation of some salient features of the 
discussion by the panel members is: 

Risk characterization should encompass the broad 
range of health effects attributable to dioxm expo- 
sure and not focus just on cancer. 

Certain noncancer effects, including changes in 
endocrine function associated with reproductive 
function in animals and humans, behavioral effects 
in offspring of exposed animals, and changes in 
immune function in animals have been demonstrat- 
ed. Some data suggest that these effects may be 
occurring in people at body burden levels that can 
result from exposures at, or near, current back- 
ground. 

While recent epidemiology studies indicate that 
dioxin and related compounds may be carcinogenic 
in humans, a focused review of these studies by a 
panel of epidemiologists is required. The Agency 
should then reconsider its current classification of 
dioxin which is based primarily on the results of 
laboratory animal studies. 



Based on the key role of the Ah receptor in mediat 
ing toxic responses to dioxin and related com 
pounds (other dioxins, furans and biphenyls) thi 
full range of compounds which bind to this recep 
tor should be considered in the risk charactenza 
tion. Additional work will be required to bettei 
understand the impact of dioxin-like PCBs 

Risks from the ubiquitous background levels of 
dioxin in the general population need to be care- 
fully considered. M- 



The PSR Qujnerlv, Sepiemher I'luj. 



Oioxin and Its Ertects on Reprixiuciive Svsiems 



432 



1. Muirav Fl, Smith FA. Nitschke KD. Humiston CG. Kociba 
R/, Schwetz BA Three-generation reproduction studv of 
rats given 2,3,7.8-(etrachlorodibenzo-p-dio«in ITCDD) in 
the diet. Toxicol Appl Pharmacol 1979:50:241-252. 

2. .Mably TA, Moore RW. Bjerke DL, Peterson RE The male 
reproductive system is highly sensitive to in utero and lac- 
tational 2,3,7,8-tetrachlorodibenzo-p-dioxin exposure In: 
Callo -MA, Scheuplein RJ, van der Hei|den CA, eds. 
Biological basis for risk assessment of dioxins and related 
compounds Banbury Report 35. Plainview. NY: Cold 
Spring Harbor Laboratory Press, 1991:69-78. 

3 Mably TA, Moore RW, Peterson RE. In utero and lactational 
exposure of male rats to 2J,7,8-tetrachlorodib«nzo-p-diox- 
in: 1 Effects on androgenic status. Toxicol Appl Pharmacol 
1992:114:97-107. 

4. Mably TA, Moore RW, Coy RW. Peterson RE. In utero and 
lactational exposure of male rats to 2J,7,8-tetrachiorodiben- 
zo-p-dioxm: 2. Effects on sexual behavior and the regulation 
of luteinizing hormone secretion in adulthood Toxicol 
Appl Pharmacol 1992:114108-117 

5. Mably TA, Bjerke DL, .Vloore RW, Cendron-Fitzpatnck A, 
Peterson RE In utero and lactational exposure of male rats 
to 2J,7,8-tetrachlorodibenzo-p-dioxin: 3. Effects on sper- 
matogenesis and reproductive capability. Toxicol .^ppl 
Pharmacol 1992,114:118-126 

6 Bowman RE, Schantz SL, Weerasinghe VC.A, Gross M, 
Barsotti D Chronic dietary intake of 2,3.7,8-tetra- 
chlorodibenzo-p-dioxin (TCDD) at 5 or 15 parts per tnllion 
in the moiJcev: TCDD kinetics and dose-etfect estimate of 
reproductive toxicitv. Chemosphere 1989:18 243-252. 

7. Egeland C, Sweeney M, Fingerhut M, Halpenn W, Willie K, 
Schnorr T. Serum dioxin (2,3,7,8-TCDD) and total serum 



testosterone, and gonadotropins in occupationally exposed 
men. Abstract presented at the Society tor Epidemiologic 
Research Annual .Meeting; June 1992; Minneapolis, .MN 
(National Institute for Occupational Safety and Health. 
Cincinnati, OH 45226). 
8. Wolfe WH, .Michaiek |E, .Miner RH, et al. The Air Force 
health study: an epidemiologic investigation of health 
effects in Air Force personnel following exposure to herbi- 
cides, serum dioxin analysis of 1987 examination results. 
Chemosphere 1992:25 213-216. 
9 Stanley js, Orban ). Chlonnated dioxins and turans in the 
general US population: NHATS FY87 results 1991. 
Washington, DC: US Environmental Protection Agency 
publication USEPA 560/5-91-003 

10. Schecter A. Dioxins and related compounds in humans and 
in the environment. In: Gallo MA. Scheuplein RI. van der 
Heijden KA. eds. Biological basis tor nsk assessment of diox- 
ins and related compounds. Banbury Report 35. Plainview, 
NY: Cold Spring Harbor Laboratory Press, 1991 169-212 

11 Piadtelli LA, Sweeney M, Fingerhut MA. et al. Serum lev- 
els of PCDDs and PCDFs among workers exposed to 
2,3,7,8-TCDD contaminated chemicals. Chemosphere 
1992:25:251-254. 

12. Bowman RE, Schantz SL, Gross ML. Ferguson SA. 
Behavioral effects in monkeys exposed to 2,3.7,8-TCDD 
transmitted maternally during gestation and tor four 
months of nursing Chemosphere 1989;18:235-242, 

13 Mori T, N'agasawa H Toxicity ot hormones in pennatal 
Life. Boca Raton: CRC Press, Inc.. 1988 

14. Kind F Hormone toxicity in the newborn. .New York: 
Spnnger-Verlag, 1990. 

15. .MastTOiacovo P. Spagnolo A. .Mami E. et al. Birth defects in 
the Seveso area after TCDD contamination. JA.VIA 
1988;259:1668-1672 



433 



Arkansas Democrat-Gazette (Little Rock), <illll^2 



Dioxin exposure study 
shows brain impairment 
in 14 Times Beach babies 



BY SANDY DAVIS 



Results of a study of 14 chil- 
dren whose mothers resided in 
dioxin-contaminated Times 
Beach, Mo., while they were 
pregnant shows the children 
have "clearly defined exces- 
sively abnormal brain mea- 
sures." 

Dr. Peter Kahn. a professor 
at Rutgers University in New 
Jersey and one of nine re- 
searchers and authors of the 
1992 study, said Tuesday the 
study revealed the bilateral 
frontal areas of the brain were 
"most significantly impaired" 
in the seven boys and seven 
girls tested. 

Kahn said that when the bi- 
lateral frontal areas of the brain 
aren't functioning normally, it 
"affects intellectual processes 
indirectly by altering states of 
r.rousal. motivation, affective 
states, and attention." 

Kahn. who also is serving as a 
consultant to a dioxin exposure 

study conducted in Jacksonville, 
called the results of the Times 
Beach study "striking and dra- 
matic." 

However, Kahn said, people 
in Jacksonville, which has three 
Superfund sites that contain 
dioxin-contaminated wastes, 
should not "panic." 

The study, which Kahn said 
was privately funded, blamed 
exposure to 2,3,7,8-TCDD, the 
most toxic form of dioxin ac- 
cording to the federal Environ- 
mental Protection Agency, for 
the brain dysfunctions in the 
children. 

"This study indicates that ex- 
posure to TCDD in utero and 
postnatally induces neurophys- 
iological dysfunction in the bi- 
lateral frontal lobes," the study 
concluded. 

In addition, the researchers 
also found that the girls tested 
"exhibited more dysfunction 
than the males. ' and explained 
that this could have occurred 



because "the hormone-like ac- 
tivities of TCDD have a greater 
effect on the developing fe- 
male." 

The children in the study 
were compared to an "age- and 
sex-matched normal popula- 
tion," according to the study. 

"These kids are suffering 
neurological complications to 
the point they are learning dis- 
abled in one way or another," 
Kahn said. "All of the children 
tested were affected." 

The children were born be- 
tween 1977 and 1983 to mothers 
who resided in Times Beach 
during and at least a short time 
after their pregnancies. 

Residents of Times Beach 
were moved out by the EPA in 
1980 after it was discovered that 
dioxin contaminated wastes had 
been sprayed on the roads and 
had seeped into the yards of 
community residents. 

"A waste hauler by the name 
of Russell Bliss was in the habit 
of collecting waste oil and 
spraying it on dirt roads, horse 
arenas, truck terminals, and oth- 
er places especially in the sum- 
mer to keep down the dust," 
Kahn said of the history of 
Times Beach. 

"He also hauled still bottoms 
from a plant where dioxin was 
involved," Kahn added. "He 



mixed these still bottoms in with 
the oil and began spraying that 
on roads. He did this in Times 
Beach in 1971." 

More than 12 years later, the 
residents were relocated, Kahn 
said. 

The problem in Jacksonville 
is not that severe, he said. 

"I think the problems in Jack- 
sonville can be fixed," he said, 
referring to various methods 
that can be used to rid the city 
of the wastes. 

"There are a number of tech- 
nologies in varying degrees of 
development that could be used 
(to clean up the Jacksonville 
wastes)." 

The EPA is incinerating 
drums of dioxin-contaminated 
wastes stored at the defunct 
Vertac Chemical Corp. plant 
site in Jacksonville. The dioxin- 
contaminated wastes were the 
unwanted byproduct of herbi- 
cide manufacturing that oc- 
curred at the plant site for more 
than 30 years. 

Kahn said the study was be- 
ing submitted for scientific re- 
view to the International Sym- 
posium on Dioxin and Related 
Compounds being held in Vien- 
na, Austria, this week. 

In addition. Kahn will ad- 
dress the U.S. Senate on Oct. 21 
to recommend what kind of re- 
search needs to be done for 
Vietnam veterans who were ex- 
posed to Agent Orange, the de- 
foliant used in Vietnam that 
contained dioxin. 



— ^— 



APPENDIX 6.— RESEARCH ON TOXIC EXPOSURES 



May 5, 1994 



COk^^ 



College of Veterinary Medicine 

Dr Richard Miller and Biomedical Sciences 

Medical Follow-up Agency Fj^S7„r^°o»d^'S^ 

Institute of Medicine (303) 49i-6i87 

National Academy of Sciences ^"^ '"^' *"*^*^ 
2101 Constitution Avenue, N.W. 
Washington, DC 20418 

Dear Dr. Miller: 

This letter addresses my concern that you are appropriately informed about approaches 
for evaluating reproductive function in men, especially when evaluations are based on seminal 
quality. It is prompted by a recent discussion with Dr. Patricia Olson who is a Congressional 
Fellow working with the Senate Committee on Veterans Affairs. My perspective in the 
comments which follow is based on over 35 years experience in research on male reproductive 
function, publication of numerous studies evaluating different approaches for predicting fertility 
on the basis of seminal quality, and service as a consultant to the EPA and NIH. I also am a 
Past-President of the American Sc-' y of Andrology. 

For a number of years a portion of my research was driven by the concept that 
improved methods for evaluation of spermatozoal motility or quantifying percentages of 
abnormal spjerm would allow substantially better predictions of fertility. More recently, I have 
rethought some of the'''' issues and concluded, as have some others, that there is a serious flaw 
to this underlying premise. Conventional methods of analysis of sperm motility or sperm 
morphology, or other tests of any individual attribute of a population of sperm, in some cases 
can identify a "loser" but never can identify a "winner" with certainty. In this context, a 
"loser" is defined as an individual who is sterile or has potential fertility substantially below 
normal, and a "winner" is one who will be of average or high fertility; in both cases assuming 
a reasonably high probability of the correct prognosis. By analogy, it would be like predicting 
the winner of this weekend's Kentucky Derby back on Christmas Eve. 

The underlying basis for this conclusion is presented in a recent paper "/« Vitro 
Evaluation of Sperm Quality: An Opinion" published in the Journal of Andrology in 
December 1993 (copy enclosed) and more succinctly presented, in a manner which is focused 
exactly on the dilemma you face, in a presentation presented to the Post-Graduate Course of 
the Pacific Coast Fertility Society on April 21, 1994, in Palm Springs, CA (copy enclosed). 
Similar elements will be developed in an invitational talk scheduled for presentation to the 
British Andrology Society in Bristol, England, on November 17. 

The reason that predictions of potential fertility will remain inaccurate, except for poor 
samples, is a direct consequence of the fact that to be successful in fertilizing an egg, an 
individual spermatozoon must have each of many attribute operating in a fully functional 



435 



436 



manner. All of these attributes have not been identified, and appropriate methods are lacking 
to quantify many of those which are known. The only way that assessment of percentage of 
motile sperm could be considered a meaningful predictor of potential fertility would be to 
ignore the fact that other attributes of sperm are important in the fertilization process and 
concurrently to ignore the fact that failure of any one of many attributes could cause an 
individxial spermatozoon to be incapable of fertilizing an egg even though it swam very well. 
Clinical and other research clearly show the fallacy of this approach. The concept is 
sunmiarized succinctly in Table 2 and Figure 1 of the enclosed presentation to the Pacific 
Coast Fertility Society. Refeiring to Table 2, if one assumes that attribute A is the ability to 
swim, it is evident that swimming ability is normal in 7 of the 8 sperm listed in the upper 
portion of that table, but only the spermatozoon which has all 7 hypothetical attributes normal, 
and none abnormal, is capable of fertilizing an egg. Recognition of this feature, and that 
fertilization is a probability event will lead you to conclude, as I have, that percentage of 
motile sperm can identify losers but not winners. 

Placed in the context of sequelae to the Persian Gulf action, it means that evaluation 
only of the percentage of motile sperm in a single seminal simple for a number of individuals 
almost certainly is doomed to fail to provide a valid answer the question which I assume you 
are asking. If the question is "Did an event or events occur during the Persian Gulf action 
which caused an actual or potential decrease in fertility of males serving in that theater?" 
evaluation of sperm motility as the sole test of seminal quality cannot provide a valid answer. 
Regardless of whether the average percentage of motile sperm in a series of seminal samples 
from individuals who served in the Gulf area is equal to, greater than, or less than that of 
appropriate matched controls cannot provide an answer to the question posed. There is ample 
documentation that a population of spermatozoa may contain a high percentage of motile cells 
but yet have severely reduced fertility or, conversely, samples with a low percentage of motile 
sperm may be quite fertile. Again, the reason is that many attributes come into play. 

I suggest a multi-tiered screening approach for your consideration. The entry level 
screen would be visual or computerized assessments of percentages of motile sperm and of 
morphologically normal sperm in the seminal samples from individuals serving in the Gulf and 
an appropriately matched control group. Individuals failing to consistently pass this test need 
not under further screening because they probably will have impaired fertility. However, 
individuals passing this entry level screen should be evaluated for several other multiple and 
independent attributes, which can be measured in several hundred if not several thousand 
spermatozoa in each sample. This might be achieved by flow cytometry; transmission electron 
microscopy; and function tests which combine swimming ability, activity of enzyme necessary 
for egg penetration, and capability of sperm to bind to the egg investments. Appropriate tests 
are available, and not all are expensive. Again, individuals failing one or more tests in the 
second level screen are likely to be of reduced fertility, but individuals passing the secondary 
level screen may or may not be capable of siring children. Ideally, such individuals would be 
exposed to a tertiary level screen which might include cytogenic evaluations, capability for 
nuclear decondensation within oocyte cytoplasm, and similar tests. 

If there was a significant difference between "exposed" and control groups in the 
percentage of individuals passing both the entry and secondary level screens, that would 
provide a strong basis for a conclusion that potential fertility differed for the two populations 
of men. Even that conclusion, however, would need to be guarded because there is no method 



437 



to unequivocally establish which tests of quality for human spermatozoa, or semen, actually 
are predictive of fertility. This matter is addressed briefly in the Pacific Coast Fertility Society 
article, and in more detail in a reprint enclosed firom the Journal of Andrology, 1989. 

In the case of men who served in the Persian Gulf, I was informed by Dr. Olson that 
there is at least anecdotal evidence that the female partners of certain of these individuals 
complain of a burning vaginal sensation after ejaculation, presumably as a consequence of 
exposure of the vaginal epithelium to the mixture of spermatozoa and seminal plasma. If there 
is validity to these reports, it should be fairly simple to ascertain if the problem is associated 
with the seminal plasma or spermatozoa. Seminal plasma contains both iipoidal compounds 
and compounds capable of transporting lipids, and the plasma membrane of spermatozoa is rich 
in lipids which serve as a "sink" for lipophilic molecules. Back in the 1960's, for example, 
we found that treatment of dairy bulls with pesticides at dosages then recommended for 
treatment of barnyard insects resulted in appearance of the insecticide in the semen, from where 
it could be extracted in both seminal plasma and spermatozoa. It should be a relatively simple 
matter to obtain seminal plasma from individuals whose spouse complains of uterine "burning" 
and analyze it for the presence or absence of trace amounts of unusual organic compounds. 

I apologize for the length of this letter, but felt that brevity would preclude presentation 
of appropriate arguments that evaluation of spermatozoal motility is an insufficient test to 
ascertain if reproductive function of men serving in the Persian Gulf was affected adversely. 
I would be pleased to provide additional information or suggest individuals who could help you 
develop appropriate methodologies to ascertain if reproductive function might have been 
altered. 



yours, 




R.P. Amann 
Professor and Head 

RPA/sjv 

Enclosures 

Olson 



sylH. 



438 




1S01 L »nt MW, Suit* 

WuMn«(aiOC200a 

TdwtaMJSHIiaOO 

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i|i 



BIRTB DEBECTS AMONG VIETNAM VETERAN FATHERS 

In the late 19703, American militaiy service men who had returned from Vietnam 
had concerns about their exposure to Agent Orange and its health consequences. Special 
concerns were raised abotit birth defects. The Centers for Disease Control used the 
Metropolitan Atlanta Congenital Defects Program data firom the years 1968 to 1980 to 
study this question. As part of the study, families were interviewed about paternal 
militaiy service, and nearly 4,000 \netnam veteran Eathers were asked to rate their 
exposure to Agent Orange. Altogether, 96 types of birth defects and 105 exposure 
variables (such as age, smoking, employment, life stresses, and fertility) were considered. 

The study found that, in genera], Vietnam veteran fathers were not more likely 
than comparable fathen to have babies with birth defects. Similarly, for all defects 
combined veterans with exposure to Agent Orange did not appear to have higher risk for 
fathering babies with birth defects. However, babies bom to Vietnam veteran fathers 
likely to have had high exposure to Agent Orange had a greater risk of certain defects - 
including spina bifida, cleft lip, and certain neoplasms. Since assessing Agent Orange 
exposure is difGcult, this evidence does not prove that it causes birth defects; it does 
provide chies "about things to be k)oked at further.* * 

.• 

It was the richness of the data base from the Metropolitan Atlanta program that 
made this study possible. The program had data over a long period of time, on many 
defects, and covers a whole population in an areas. More recently, questions have been 
asked about certain exposures to those who were present during xht Gulf conflict Better 
international data could provide answers to these new questions. 

The March of Dimes is concerned about environmental exposures that cause birth 
defects, whether they occur in the home, at work, or as part of military service. 

Sources; 

1. Erickson JD. et al. "Vietnam Veterans' Risks for Fathering Babies with Birth Defects" 
US. DHHS-PHS, August 1984. 

2. Erickson JD. "Risk Factors for Birth Defects: Data From the Atlanta Birth Defects 
Case-Control Study" Teratology 43:41-51 (1991) 

3. Erickson JD. et aL "Vietnam Veterans' Risks for Fatheriiig Babies with Birth Defects" 
JAMA, 252:903-912 (1984). 

May 1994 



439 



JAMA 



Original Contributions 



Vietnam Veterans' Risks for 
Fathering Babies With Birth Defects 

J. David Erickson. DOS. PhD; Joseph Mulinare, MO, MSPH: Ptiilip W. McQain. MS; Terry G. Fitch. MA; 
Levy M. James, MS; Anne 8. McCteam; Myron J. Adams, Jr. MO 



• Vietnam veterans' risks for fathering babies with major structural birth 
defects ware assessed using a case-control study. Information regarding 
military service in Vietnam was obtained from interviews with mothers and 
fathers of babies In caae and control groups and from review of military 
records. Vietnam veterans, in general, did not have an increased risk of 
fathsring babies with defects (ail types combined; relative risk estimate, 
0.97). Vietnam veterans who had greater estimated opportunities for Agent 
Orange exposure did not seem to be at greater risk for fathering babies with 
ail types of defects combined. However, for a few specific types of defects 
the estimated risks were higher for subgroups of Vietnam veterans that may 
have had a greater likelihood of exposure to Agent Orange. These seemingly 
higher risks could be chance events, the result of some experience In the 
Vietnam service of the father, or the result of some other unidentified risk 
factor. 

{JAkIA 1984:252:903-9 12) 



THIS REPORT describes the results 
of a case-control study desigrned to 
determine if men who served in the 
US military in Vietnam have been at 
increased risk of fathering babies 
with serious congenital malforma- 
tions. This study was conducted pri- 
marily because of the concern ex- 
pressed by many Vietnam veterans 
that they may have suffered from a 
variety of ailments as a consequence 
of their service there. The possibility 
of increased risks for fathering babies 
born with birth defects has been 
among the foremost of their concerns. 
A few anecdotes related to this specif- 



OiMum Oivwon. Canlw tor EnvronnwnUI HmW, 
C«it*rs Kv OnuH Control. Altanu. OA 30333 (Or 
Encluon) 

JAMA. Aug 17. 1984— Vol 252, No. 7 



ic concern have appeared in the corre- 
spondence sections of some medical 
journals,''' but until recently there 
have not been any published reports 
of studies of humans specifically con- 
ducted to address this concern.' 

Many Vietnam veterans are partic- 
ularly concerned that their problems 
(or their alleged increased risk for 
problems) stem from exposure to her- 
bicides in Vietnam, particularly the 
herbicide known as "Agent Orange." 
Agent Orange was an equal mixture 
of two herbicides, 2,4,5-trichloro- 
phenoxyacetic acid (2,4,5-T) and 2,4- 
dichlorophenoxyacetic acid.' The 
compound 2,3,7,S-tetrachlorodibenzo- 
p-dioxin (TCDD) was a synthetic con- 
taminant of the 2,4,5-trichlorophe- 
noxyacetic acid. Much of the herbicide 
used in Vietn;im was dispersed by the 
Ranch Hand Program from fixed- 



wing aircraft, but other methods of 
application were also used. 

It is well known that the exposure 
of pregnant women to certain chemi- 
cals can result in disturbed erabryo- 
gensis and consequent birth defects. 
The potential for paternally derived 
birth defects as a result of chemical 
exposures is, however, largely un- 
known. Based on current understand- 
ing of human reproduction, Fried- 
man' suggests that such exposures in 
fathers could cause birth defects in 
three ways: (1) by gene muution, (2) 
by chromosomal mutation, or (3) by 
acting as a teratogen carried in the 
semen. The potential for Agent 
Orange or TCDD causing birth de- 
fects by one or more of these mecha- 
nisms is unknown. 

Despite the special concern with 
herbicide exposure, however, this 
study was designed primarily to 
determine if Vietnam veterans (in 
general) have been at increased risk. 
This approach was taken because at 
the time the study was designed it did 
not seem to be possible to obtain any 
measure of herbicide exposure except 
by questioning individual Vietnam 
veterans. 

METHODS 
Selection of Cases and Controls 

This study was based on the experiences 
of parents of selected babies born in the 
metropolitan AtlanU area during the 
years 1968 through 1980: these babies are 
referred to as "index" babies Because it 
was through them chat the study parents 

Vietnatn Veterans— Etickson et al 903 



440 



wer« identified. The index babies in the 
cajc group were those (live bom or still- 
bom) with serious structural congenial 
malformations (birth defects) and regis- 
tered by the Metropolian Atlanta (Con- 
genital Defects Program (MACDP) (the 
MACOP does not register other advene 
reproductive outcomes such as Infertility, 
spontaneous abortion, and physical or 
mental deficits that only become apparent 
later in childhood). This program attempts 
to ascertain all babies with defects diag- 
nosed daring the first year of life bom to 
mothers resident in the area.' In all, about 
13.000 babies with birth defects bora dur- 
ing Che years 1968 through 1980 were 
registered by the MACDP. Many of these 
babies had abnormalities usually classed 
as minor anomalies (eg, ear tags, hydro- 
cele, or some forms of Polydactyly). In 
order that this study be completed as 
quickly as possible, the babies in the case 
group were chosen only from among those 
who had defecU coded by InUrnational 
CloBtifieation of DiatoM, eighth revision 
fICD-8),' rubrics that usually signify seri- 
ous or major birth defects. A serious 
defect was defined as one that could be 
associated with premature death, cause 
substantial handicap, or require surgery 
or extensive medical care. This selection 
process resulted in the initial choice of 
7.529 babies in the case group from among 
the 13,000 registered. The final number 
eUgible for the study was 7.133 (Table 1). 
This reduction occurred for various rea- 
sons, including the exclusion of babies 
thought to have been given up for adop- 
tion, the random choice of one baby from 
families with more than one registered 
baby, and the selection of babies for a pilot 
study. 

The index babies in the control group 
were selected from among the 323.421 
babies who were live bom in the Atlanta 
area during the years 1968 through 1980. 
These babies were selected with the aid of 
the SUU of Georgia Vital Records Unit. 
The babies were chosen so that they were 
approximately frequency matched to the 
babies in the case group with respect to 
the following characteristics (sampling 
design variables): race (white and other). 
year of birth, and hospital of birth (20 
hospitals). Some of the babies thus chosen 
were index babies from the case group, 
and these were deleted from the control 
group (and retained in the case group). 

The power (ie. ability) of a study to 
detect increased risks for fathering babies 
with defects depends on the magnitude of 
the true risk, the number of cases avail- 
able, the number of controls available, the 
rate of the exposure of interest in the 
control group, and the level of significance 
chosen. The frequency of the major "expo- 
sure" variable of interest— the proportion 
of Vietnam veUrans among the fathers of 



by Case-Gonirot Statue. Race. 



6.13a 


Ml 3 C74) 


3.384 (88) 


3.04« 


2.301 (78) 


2.008 (88) 


•.1W 


8.114 (78) 


8,300 (88> 


1.9B7 


1.118 (88) 


SM m» 


1.200 


728 (81) 


420 (36) 


».1«7 


1*14 (88) 


1,013 (32) 


r,tss 


4.9M (88) 


3,877 (66) 


4.448 


3.028 (71) 


2.428 (67) 



3J0S (82) 
1.807 (63) 
6,100 (83) 

637 (27) 
372 (31) 
000 (28) 

3,738 (6B 
2.278 (64) 
8,010 (63) 



babies born without defects— was not 
known at the time the study was designed, 
but estimated to be 10% to 20%, based on 
information provided by the Atlanu office 
of the Veterans Administration. Estima- 
tions of statistical power baaed on the 
number of babies in the case group avail- 
able from the registry and on the esti- 
mates of the frequency of Vietnam veteran 
fathers showed that little was to be gained 
by including more than about 3.000 babies 
in the control group. For this number of 
controls, coupled with the number of avail- 
able babies in the case group, the power 
would be about 70% to detect an odds ratio 
(OR) of 1.2 for all types of birth defects 
combined and almost 100% to detect ORs 
of 1.5 or greater (two-tailed x' test for 2 by 
2 tables; a-O.OS). Adding more controls 
would not increase the power for detecting 
increases or decreases for all types of 
defects combined commensurate with the 
increased study time or expenditure 
required to include them. Moreover, the 
power to detect increased or decreased 
risks for specific types of defects was 
expected to be low, except for rather large 
relative risks (eg, 3.0). In such insUnces. 
the addition of controls above 3.000 would 
result in almost no gain in power. After a 
pilot study provided an estimate of partici- 
pation rates (70%), 4,246 families in the 
control group were selected as being eligi- 
ble for the study (Table 1). 

Study DaU 

Information about the families of babies 
in the case and control groups was gath- 
ered during interviews with the babies' 
mothers and fathers during the years 1982 
and 1983; interviews were done using a 
computer-assisted telephone interviewing 
system. Before the parents could be inter- 
viewed, they had to be located. This loca- 
tion process began with information chat 
was recorded, at the time of Che babies' 



birth, on birth certificates or MACDP 
records. With the exception of names, 
much of the available information (eg. 
addresses) was not current when the study 
was done. As a result, locating parents was 
difficult and required the use of various 
locating sources. Care was taken Co ensure 
chat the information used could be applied 
equally to families in the case and control 
groups, and that the tracing staff should 
not be aware of the case or control status 
of the families. When parenU were con- 
tacted, they were asked to participaU in a 
study designed to help learn about Che 
causes of birth defects— no specific men- 
tion was made of Agent Orange or service 
in Vietnam. 

E^h mother and father who was willing 
to participate was interviewed by two 
incerviewers. The firsC interviewer for 
each parent asked about the parent's 
reproductive history. Because such history 
would include a description of the health 
of the index baby, Che first interviewer 
could usually not avoid knowing whether 
Che index baby belonged Co Che case or 
control group. Then, so that interviewer 
bias mighc be avoided, a second inur- 
viewer for each parent asked questions 
about a wide varieCy of exposures (eg. 
occupacions. chronic diseases, and drugs; 
questionnaires are reproduced in a report 
by Erickson et al') and had no opportunity 
Co know Che case- or conCrol-group status 
of the index baby. In all, four different 
interviewers had concact with a family if 
both the mother and the father completed 



Special emphasis was given Co obtaining 
a hiscory of paternal military service. For 
this study, a veteran was defined as a 
father who had served in Che US miliUry 
ac any time in his life, and a Vietnam 
veteran was defined as a father who had 
served in Vietnam in the US miliUry 
before Che conception of his index baby. 



g04 JAMA. Aug 17. 1984— Vol 2S2. ^4o. 



Vwtnam Veteran*— Erickson « 



441 



E«ch Vietnun veteran WM asked if he 
believed he had been ezpoaed to Agent 
Orange. 

The Army Agent Orange Task Force 
also gave most Vietnam veterans a graded 
score reflecting their estimated opportuni- 
ties for exposure to Agent Orange. The 
Exposure Opportunity Index (EOI) score 
was the result of a generally subjective 
evaluation made by a panel of service 
specialists on the basis of a veteran's 
occupation, location, and time of service in 
Vietnam; these specialisU were familiar 
with the existing records of herbicide 
applications (records that document the 
time, place, and amount of herbicide used) 
and took them into account in the scoring 

Some occupational and service groups 
were thought to have had mora opportuni- 
ties for exposure than others. For exam- 
ple, ground troops were much more likely 
to have had opportunities for exposure 
than, for example, shipboard personnel. In 
addition, veterans of the same branch of 
service with similar occupational speciali- 
ties might have had different opportuni- 
ties for exposure, depending on when and 
where they served in Vietnam. Most of the 
EOI scoring done for Vietnam veterans in 
this study required specific, detailed 
review and discussion of the particular 
circumstances; some examples can be 
found in the comprehensive report on this 
study.' 

The EOI evaluations were done without 
knowledge of case or control status. Two 
separata EOI scorings were done— one 
based on occupation, location, and time 
recorded in military records, and the other 



from Vietnam 



during the inter- 



The accuracy of Vietnam veterans' self- 
reports of Agent Orange exposure is 
unknown, as is the accuracy of the EOI, 
and it is unlikely that any validation will 
ever be possible. The records of troop 
movements and herbicide use that are 
available today were made for military 
purposes and not for the purpose of esti- 
mating exposure for epidemiologic studies. 
Nevertheless, at the time this study was 
designed, it was not thought possible to 
obtain any measure of Agent Orange expo- 
sure except by questioning Vietnam veter- 
ans themselves. 

Analytic Approach 

The birth defects that affected the index 
babies in the case group were categorized 
into 96 groups for the purpose of analysis. 
Some of the 96 groups were specified by 
individual ICD-i codes and others by vari- 
ous combinations of codes, including one 
group comprising all case babies (ie, all 
types of defects combined). A baby with 
more than one defect contributed one 

JAMA. Aug 17. 1984— Vol 252. No. 7 



observation to each relevant-defect group. 
A special group consisting of babies whose 
defects were probably caused by a fresh 
dominant muution was alao formed. 

Within each of the 96 defect groups four 
hypotheses were tested: 

1. Veteran Statua.— This was an evalua- 
tion of whether the risks of veterans for 
fathering babies with birth defects were 
different from those of nonveterans. The 
primary purpose of testing this hypothesis 
was to evaluate the possibility of a 
"healthy soldier" effect, although the pos- 
sibility of increased risks was also enter- 
tained. Stodies have shown that ' 
tend to be healthier than their i 
counterparta.' This better health may or 
may not extend to reproductive health; no 
studies on the subject have been done. 
Testing the hypothesis seemed worthwhile 
because Vietnam veterans could possibly 
be at increaaed risk ralative to other 
veterans but at decreased risk relative to 
nonveterans. For each defect group, if the 
test statistic for the hypothesis was signif- 
icant (?<.0S), and the OR estimate of the 
relative risk was leas than 0.83 (or greater 
than iu reciprocal, 1.20), the dau for the 
tests of the remaining three hypotheses 
were limited to veterans. 

2. Vietnam VeUran Sutus.-The evalu- 
ation of the hypothesis that the risk of 
Vietnam veterans was different from that 
of other men waa the primary purpose of 
this study. 

3. Agent Orange Exposure Opportunity 
Index.— The aasesament of the possibility 
^hat the risk of fathering a baby with a 
defect was related to the EOI scores was 
ass es s ed twice, once by using the EOI 
based on information derived from mili- 
tary records, and once by using the EOI 
derived from information provided by 
Vietnam veterans during the interviews. 

4. Self-reports of Agent Orange Expo- 
sure.— The frequency of self-reported 
Agent Orange exposure was evaluated. 
Many persons will question the ability of 
Vietnam veterans to give accurate answers 
to the question of Agent Orange exposure, 
believing that there is a substantial possi- 
bility for response bias connected with 
case-control status. In other words, it is 
possible that men who have fathered 
babies bom with defects may have 
searched their memories for possible 
causes of those defects. Differential 
reporting would result in biased estimates 
of risk. To reduce the possibility of such 
bias, the protocol for this study called for 
evaluating this hypothesis by comparing 
dau on one type of defect with data on all 
other types of defecU. This approach 
requires the assumption that the exposure 
of interest does not cause an increase in all 
or most types of defects. 

Each of the hypotheses for each defect 
group was evaluated three times; each of 



the three evaluations was done with the 
data stratified on the sampling design 
variables (the variable, year of birth, was 
combined into three S2-month periods). 
First, risk estimates wera made without 
consideration of potentially confounding 
variables (except for the sampling design 
variables). Second, risk estimates were 
made in which consideration was given to 
four eovariables identified (before data 
analysis) by a group of specialists in birth 
defects as being particularly important. 
These four eovariables were maternal age, 
maternal education, matarnal alcohol con- 
1 the occurrence of birth 
defects in firat-degree relatives of the 
index babies. And third, consideration was 
given to 108 eovariables. 

The major analytical tool for the tests of 
hypotheses was conditional logistic regres- 
sion." A positive regression coefficient 
implies increasing risk and a negative 
coefficient implies decreasing risk. In 
addition, a logistic regression coefficient 
can be transformed into ORa. and an OR 
can be used ss an estimste of relative risk. 
A relative risk is the ratio of two risks. 
For example, if Vietnam veterans had 
twice the risk of having babies with birth 
defects relative to other men, their rela- 
tive risk would be 2.0. Likewise, if Vietnam 
veterans' risk was half that of other men, 
their relative risk would be 0.5. 

Different subseu of the complete daU 
were used for the vsrious tests of hypothe- 
ses. For the analyses done without con- 
sideration of potentially confounding 
variables (except the sampling design var- 
iables), the following subsets were used: 
(1) Data taken from mothers' interviews 
wera used for the Veteran Sutus and 
Vietnam Veteran Statua hypotheses. This 
waa done because mora mothen than 
fathera were interviewed, and because 
mothen' answera were shown to sgree 
closely with fathera' answen (where both 
mother and father were interviewed) to 
the questions regarding the fathera' veter- 
an and Vietnam veteran status'; and (2) all 
fathera' interviews were used for the 
hypotheses concerning Agent Orange ex- 
posure because mothen were not good 
substitutes for fathen insofar as this 
issue was concerned and, furthermore, 
because they were not fully questioned 
about the issue. For the analyses that took 
account of potentially confounding varia- 
bles, the data were (for the most part) 
derived from mothen' and fathen' inter- 
views from families in which both the 
mother and father completed interviews.' 

Three supplementary issues related to 
military service in Vietnam were also 
evaluated: 

1. Vietnam Veteran Birth Defect Syn- 
drome.— The data were analyzed to see if 
the fathen of babies with particular com- 
binations of defecU were more frequently 

VMtnam Vaterans— Ericfcson st al 905 



442 



Vietnam veterans than were the fathers of 
hdex babies in the control group. Combi- 
nations of pairs and triplets of ICDS 
defect codes were evaluated. For example, 
the frequency of Vietnam veterans among 
the fathers of babies with the defect-pair 
anencephalus and omphalocele was com- 
pared with the frequency among the 
fathers of index babies in the control 



thering Several Affected Babies.-The 
possibility that Vietnam veterans have 
had a persistent increased risk of 
fathering more than one baby with birth 
defects was evaluated within the case 
group as follows: the frequency of defects 
in siblings bom after the index babies of 
Vietnam veWran fathers was contrasted to 
the frequency in later-bom siblings of 
index babies whose fathers did not serve 
in Vietnam. 

3. Malaria and Malaria Chemoprophy- 
laxis.— Each interviewed Vietnam veteran 
father was asked if he had contracted 
malaria while he was in Vietnam; each 
was also asked if he had taken medicines 
for preventing malaria. This was the only 
health-related issue about which Vietnam 
veterans received special questioning- 
there were no queries about other diseases 
that men may have contracted in Vietnam. 
The controls for the fathers of babies with 
a particular type of defect were the 
fathers of babies with all other types of 
defects (this was done for the same reason 
as mentioned herein in reference to the 
use of the technique for evaluating self- 
perceived Agent Orange exposure). 

RESULTS 

Overall, 69.9% of eligible mothers 
and 56.3% of eligible fathers com- 
pleted interviews (Table 1), and an 
additional 1% or so of mothers and 
fathers partially completed inter- 
views to the point that a paternal 
military history was obtained.' The 
participation rate for parents of the 
white race was subsUntially higher 
than that for parents of other races, 
particularly for fathers (Table 1). No 
notable differences in the case-con- 
trol participation rates were noted for 
white parents, but for parents of 
other races the control-group partici- 
pation rates were about 5% higher 
than those for the case group (Table 
1). This difference was shown to be of 
little concern insofar as it might 
affect the inferences to be drawn 
regarding the risks of Vietnam veter- 
ans.' With stratification on race, 
there was equal participation of fami- 
lies in the case and control groups 



Table 2 —Veterans' and Vietnam Veiefana' Risks tor 
Famehng Babws With Birtn Detects* 


Gfoup 


Velwan Falt>er*,t Menvelwan Faltwn, 
Ne. (%) Mo. (%) 


Total. 
Ne. (%) 


Coom^BTOuo 


I.SS9 (3S) 
1.047 (39) 


2.727 (82) 
1.652 (61) 


4.}88«100) 
2.699 (100) 


Grew 


tutk* lot 

Fattwra. 
No. (%) 


VIellun VetersiM' 

AiOthef 
Father*. 
Me. (%) 


Total. 
No, (%) 


Ca*. group 

Coo«.flro«, 


428 (9) 
268 (9) 


4.3e7«9i) 
2.699 (91) 


4,815 (100) 
2.967 (100) 




TaWe 3.-Birth Defects Risks a 


nd Afleflt Oinge Exposure Opportunity Indicee' 


Index 


Scoot 


CaeeOroee. 
Mo. (%) 


Ceelrel Oroee. 
Nd. {%) 


intto Kcarding lo mlonnelion 
oMMwd Irom mmmr, reconut 




3.606 (92) 
121 (3) 


2.200 (93) 
73(3) 






60 (2) 


31 (0 






54 (t) 


34(1) 






40 (1) 


18 «t) 






44 (1) 


23(1) 


Total 




3.924 (100) 


2.379 (100) 


index KCOnSng lo .nh»m.l>on 
oMM dunog .m«v».i 




3.606 (91) 
1 18 (3) 


2.200 (92) 
78 (3) 






70 (2) 


46 (2) 






79 (2) 
S3 (1) 


41 (2) 
23 (1) 






26 «1) 


14 «1) 


Total 




3.9S1 (100) 


2.402 (100) 




with respect to the other sampling 
design variables: year of birth and 
hospital of birth. In addition, there 
was relatively little variation in the 
participation rates for families in the 
case group associated with the type of 
defects that affected the index babies. 
Roughly 50% of the fathers of 
white index babies were said by the 
mothers to have served in the mili- 
tary, in contrast to about 30% of 
fathers of other race index babies. 
About 9% to 10% of fathers of white 
index babies were said by mothers to 
be Vietnam veterans as compared 
with 6% to 7% of fathers of other 
race index babies; again, there was 
not much difference in the case- and 
control-group rates. As sUted by 



Aug 17. 1984— Vol 252. No 7 



mothers, about 2% of white fathers 
could not be classified as to whether 
they were Vietnam veterans as com- 
pared with 6% to 7% of other race 
fathers. Slightly more than 10% of 
interviewed white fathers said that 
they were Vietnam veterans, and the 
percentage for interviewed other race 
fathers was about the same. The fact 
that there was not a higher propor- 
tion of other race fathers who were 
Vietnam veterans, as compared with 
white fathers, may surprise some 
readers. It is popularly believed that 
a disproportionate number of black 
men served in Vietnam. We now 
know, however, that this was not the 
case, although those black men who 
did serve there may have borne a 

Vietnam Veterans— Erickson et al 



443 



somewhat heavier burden of com- 
bat." 

Estimations of the relative risks 
(OR estimates) for veterans and Viet- 
nam veterans for fathering babies 
with all types of defects combined are 
presented in Table 2 (these analyses 
took account of the sampling design 
variables, but not of other potentially 
confounding variables). There were 
1,659 fathers of babies in the case 
group and 1,047 fathers of babies in 
the control group who were veterans 
(excluding Vietnam veterans) and 
2,727 fathers of babies in the case 
group and 1,652 fathers of babies in 
the control group who were not veter- 
ans. The OR (relative risk) as esti- 
mated by logistic regression using the 
maximum likelihood method is 0.94, 
with 95% confidence limits of 0.85 to 
1.04. Thus, there is no evidence in 
favor of the position that veterans 
(excluding Vietnam veterans) have 
had a different risk for fathering 
babies with the aggregate of the birth 
defects studied here. Because there is 
no such evidence, the tests of the 
remaining hypotheses made compari- 
sons of the frequency of Vietnam 
veterans (and subsets of them) with 
nonveterans as well as other veter- 
ans. The OR for Vietnam veterans 
fathering babies with defects is 0.97, 
not significantly different from 1.0 at 
the 95% confidence level (Table 2). 
Therefore, there is no support in 
these data for the proposition that 
Vietnam veterans (in general) have 
been at different risk than other men 
for fathering babies with the types of 
birth defects that we studied. 

The distributions of Vietnam veter- 
ans on the two variants of the EOI 
are presented in Table 3 (a score of 1 
indicated minimal opportunities for 
exposure: 5, the highest opportunities; 
and scores of 2, 3, and 4, graduated 
intermediate opportunities). Among 
those who were classified on both 
variants, 52% received the same 
score, and about 84% received the 
same score plus or minus 1. For each 
of the two EOI variants a logistic 
regression model was fitted. In both 
cases the resultant regression coeffi- 
cients were not significantly different 
from (Table 3), indicating no evi- 
dence for either an increase or a 
decrease in the risk for fathering 
babies with birth defects related to 
the EOI scores. 

JAMA. Aug 17. 1984—70) 252. No. 7 



About 25* of interviewed Vietnam 
veterans believed that they had been 
exposed to Agent Orange, whereas 
roughly the same proportion said that 
they did not know if they had been 
exposed. For the defect group "All 
Case Babies," no tests of hypotheses 
regarding self-reported exposure to 
Agent Orange were done. As de- 
scribed previously, the frequency of 
self-reported exposure was assessed 
only among the fathers of babies in 
the case group, and as the name of the 
group "All Case Babies" implies, no 
control group was available. However, 
the tests were done for all other 
defect groups. 

The tests of hypotheses for the 
remaining 95 defect groups are pre- 
sented in an abbreviated form in 
Table 4. As an aid to the reader in 
interpreting Table i_, the results for 
the group "All Case Babies" pre- 
sented in Tables 2 and 3 are repeated 
in Table 4. The OR estimates for the 
tests of hypotheses regarding risks 
associated with self-reported expo- 
sure to Agent Orange are also pre- 
sented in Table 4; for example, for the 
defect group "Multiple Defects" the 
relative risk estimate was 1.07, not 
significantly different from 1.0 
(P>.05). 

For the most part, the tests of 
hypotheses for the remaining 95 
defect groups (Table 4) yielded results 
similar to those just described. Some 
important departures from the gener- 
al finding of no different risks for 
Vietnam veterans (and subsets of 
them) will be described. Some statis- 
tically significant findings are not 
described but can be identified in 
Table 4, and still others can be found 
in the comprehensive report on this 
study.' 

The estimated risks for fathering 
babies with spina bifida are higher 
for Vietnam veterans with the higher 
EOI scores. The 20 Vietnam veUran 
fathers of babies with spina bifida 
who received scores on the EOI 
derived from information contained 
in military records were distributed 
as follows: score 1, five fathers: score 
2, four fathers; score 3, six fathers; 
score 4, three fathers; and score 5, two 
fathers. The distribution of Vietnam 
veteran fathers' scores on the inter- 
view-derived EOI was 3, 2. 6. 7, and 1 
for scores of 1 through 5, respectively. 
The regression coefficient for the 



first EOI implies ORs of 1.2, 1.4, 1.6, 
1.9, and 22 for scores of 1 through 5, 
respectively, and the coefficient for 
the second EOI implies ORs of 1.2, 1.5, 
1.8, 2X and 2.7. 

Veterans had a higher estimate*? 
risk for fathering babies with cleft lip 
with or without cleft palate, as did 
Vietnam veterans who had higher 
scores on the second EOI; the distri- 
bution of Vietnam veteran fathers 
was 8, 7, 1, 4, and 5 for scores of 1 
through 5, respectively. The regres- 
sion coefficient implies ORs of ISi, 1.4, 
1.6, 1.9, and 2.2 for scores of 1 through 
5, respectively. 

Vietnam veterans with higher 
scores on the second EOI had higher 
estimated risks for fathering babies 
with "Other Neoplasms"; the distri- 
bution of fathers was 4, 4, 3, 2, for 
scores of 1 through 5, respectively. 
The coefficient implies ORs of 1.3, 1.7, 
2.2, 2.8, and 3.7. The estimated risk for 
the Vietnam veteran hypothesis had 
95% confidence limits of .99 to 3.29. 
The neoplasms classified in this 
group include (for Vietnam veteran 
and all other fathers) dermoid and 
epidermoid cysts (26 cases), terato- 
mas (14 cases), lipomas (nine cases), 
hamartomas (five cases), CNS tumors 
(five cases). Wilms' tumors (three 
cases), neuroblastomas (three cases), 
hepatoblastoma (one case), rhabdo- 
myosarcoma (one case), and miscella- 
neous benign tumors (24 cases). 

The analyses in which the potential 
confounding effects of covariables 
were evaluated gave results very sim- 
ilar to those just presented, indicat- 
ing that the covariables were not 
important confounding variables in 
this study. The only substantial 
departure from this general picture 
was that Vietnam veterans had sig- 
nificantly lower estimated risks for 
fathering babies with defects classed 
in the group "(Complex Cardiovascu- 
lar Defects" when consideration was 
given to those covariables identified 
as being particularly important be- 
fore analysis (OR, 0.59). 

In seven families in the case group 
the father stated that he had. been 
exposed to Agent Orange and the 
mother reported birth defect-affected 
siblings born after the index baby; 
this was a significantly higher num- 
ber than expected on the basis of the 
frequency in other families in the 
case group (OR, 2.57). No striking 

Vietnam Veterans — Ericfcson at al 907 



444 






i^fe^'^^- 



...r^aCV -^_ 








i.otz 



in»5«iT'3g?:,";;T 







2.5S 

0.78 



-007 -OLIO 

o.ta ojo 



CIS 0.16 

0.18 0.18 



-0.47 -0.1J 



097 

0.84 





0.11 


-0.21 


3.48 


024 


04a 




-0.70 


-0.8I 


toe 


-0.10 


-0.01 




OIO 


022 


149 


-0J8 


0.07 


0.8 1 


0.02 


-i.oa 


1.01 


0.06 


0.03 


OM 


0.02 


-0.07 


024 


0.05 


0.04 


0.89 


-O.OS 


-001 



7 
131 



-0.09 -o.oe 

-007 -004 



-009 -003 

-047 -0.08 

008 0J6 

0.00 0.00 



)22 



JAMA. Aug 17. 1984— Vol 252. No ^ 



Vietnam Velerans— Erickson el < 



445 



":^^^v>:' 










40 0.82 1. 10 0.94 a 13 -0.02 



>:S3 


i::^::^:^:.^.::^::::::::^^} 


!=3i-i£^5l 


aa 


OM Ija 0.M 


0.06 -0.06 


.:v'^-*j 


.:^:^::;:::'^i-«:^^rB^.i 


■■.r^^-T-^S^ 


4« 


1.42 O.M 


-0.06 0.00 


•*. '.'S 


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M7 


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-0.02 0.01 


1« ■^'i 


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. .fl[.u;!;..ao»»: 


21 


1.11 2M I.S3 


0.16 0.32 


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~:r. " ".T-:*^ 






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' .*v-".->1:V?R{ 








13 


0.64 J.01 8.8S 


0.48 


:^:::^ 


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OM r£ig^ 



26 0.80 0.74 . . . 0.02 0.14 




-0.81 -0.94 



09 I 



JAMA. Aug 17. 1984— Vot 252. No. 7 Vielnam Valcrans— Erickson •! al 909 



83-529 95-15 



446 



"syndrome" of defects (baaed on com- 
binations of ICD-8 codes) was found 
among the babies in the case group 
born to Vietnam veterans. 

Fathers of babies born with defects 
classified in the 'Total Sex Organ 
Defects" group were more likely to 
have said that they had contracted 
malaria while they were in Vietnam 
than were the fathers of other babies 
in the case group (OR, 3.44; 95% 
confidence limits, 1.60-7.41; 11 out of 
246 fathers of babies with sex organ 
defects reported malaria in contrast 
to 20 out of 1,537 fathers of babies 
with other defects). The results were 
very similar for the group "Hypo- 
spadias," which accounted for most of 
the babies classified in the former 
group. No associations were found 
between the occurrence of defects and 
reported use of antimalarials. 

COMMENT 

The most important conclusion to 
be drawn from this study is that the 
data collected contain no evidence to 
support the position that Vietnam 
veterans have had a greater risk than 
other men for fathering babies with 
all types of serious structural birth 
defects combined. Many fathers, 
whether Vietnam veterans or not, 
have had the misfortune of having 
babies with birth defects. Although 
specific types of structural birth 
defects are rare, when all types are 
combined they usually affect roughly 
2% to 3% of stillborn and live-born 
babies. A large number of American 
men served in Vietnam— 2.6 million 
as estimated by the Veterans Admin- 
istration." Because most of these men 
were quite young when they served, a 
large number of babies will have been 
born to them during the past 15 years 
or so. If these men have had an 
average of one baby each since the 
time of their service, they will have 
had 52,000 to 78,000 babies born with 
serious defects if they have had the 
usual risk of 2% to 3% . If these men 
have had an average of two babies 
each, then these figures would be 
doubled. Although these numbers 
may seem alarming, they are based 
on nothing more than assumptions 
about the fertility of Vietnam veter- 
ans and the usual rate at which birth 
defects occur. 

This study cannot prove that some 
factor associated with service in Viet- 



nam was or was not associated with 
the occurrence of rare types of 
defects, of defects in the babies of 
selected persons, or of defects in the 
babies of small groups of veterans. 
However, the conclusion that Viet- 
nam veterans in general have not 
fathered babies with all types of birth 
defects combined, at higher rates 
than other men is based on relatively 
strong evidence. This study has not 
identified the causes of the birth 
defects that have occurred in the 
babies of Vietnam veterans, nor in 
the babies of men who did not serve 
in Vietnam. The causes of the vast 
majority of birth defects remain 
unknown. Two to three percent of the 
babies born to Vietnam veterans in 
the future will have serious birth 
defects, just as will a similar propor- 
tion of babies born to other men. The 
discovery of the causes of these 
defects, discovery that may make pre- 
vention possible in the future, will 
depend on other research. 

In addition, this study does not 
provide support to the notion that 
those men who may have been 
exposed to Agent Orange in Vietnam 
have had an increased risk of 
fathering babies with most types of 
defects. The conclusion regarding the 
lack of increased risks associated 
with Agent Orange is based on con- 
siderably weaker evidence than the 
conclusion about Vietnam veterans in 
general. 

Any study in which information is 
not obtained from all of the target 
sample engenders concern that per- 
sons who did not participate are dif- 
ferent from those who did and that 
this difference might be a source of 
bias in the study results. The main 
reason for nonparticipation in this 
study was that parents could not be 
located. Participation rates for other 
race parents were lower than those 
for white parents, particularly for 
fathers. This fact may limit our abili- 
ty to generalize the study results for 
other race fathers. However, assess- 
ments were made for the possibility 
that the risks for white and other 
race fathers varied (for each of the 
hypotheses for each of the defect 
groups), and few differences were 
found. 

The data on some of the exposures 
of interest had to be collected from 
parents, not from some external 



910 JAMA. Aug 17. 1984— Vol 252. ^4o. 7 



source. In most case-control studies, 
there is fear that members of the case 
and control groups will not give expo- 
sure histories with equal accurac\', 
thereby introducing bias into the 
case-control comparisons. For the 
main exposure in this study, paternal 
military service in Vietnam, we 
believe that there is little reason for 
concern about the accuracy of infor- 
mation reported by either parents in 
the case or control group. 

However, the ability of Vietnam 
veterans to give valid reports of expo- 
sure to Agent Orange is a matter for 
debate. In addition, some observers 
will also adhere to the position that 
only a small proportion of Vietnam 
veterans had a potential for exposure. 
Rather than enter these debates, the 
approach of this study was to listen to 
the reports of Vietnam veterans and 
to use comparison techniques that 
should reduce possible case-control 
response biases. About one fourth of 
Vietnam veterans who participated in 
this study believed that they had been 
exposed to Agent Orange. It is a 
strength of this study that their 
assessment of exposure was used in 
the analysis. The potential for bias in 
the analyses of the self-reports of 
Agent Orange exposure has presum- 
ably been reduced by using only the 
parents of babies born with defects as 
controls. However, the success of this 
technique cannot be fully known. 

The validity of the Agent Orange 
EOI is uncertain and will probably 
remain so. The records that must be 
used today to make estimates of expo- 
sure possibilities were made for mili- 
tary purposes, not for the purpose of 
conducting health studies. However, 
the index scoring for this study was 
done by service personnel familiar 
with the existing records that docu- 
ment the use of herbicides in Vietnam 
by time and place. This suff also had 
personnel files at hand from which to 
document Vietnam veterans' occupa- 
tions and military units and records 
from which to estimate the locations 
of the units at various times. More- 
over, a separate index scoring was 
done for which information on loca- 
tion and occupation was obtained 
from the men during the interviews. 
Again, use was made of information 
given by veterans, and this is consid- 
ered a strength of the study. Finally, 
the scoring was done by service staff 

Vietnam Veterans- Erickson at al 



447 



who had no knowledge of the case- or 
control-group status of the individual 
veterans; therefore, there can be no 
question about scoring biases being 
connected with case-control status, as 
there is in respect to the self-reports 
of Agent Orange exposure. 

Although the overall results of this 
study indicate that Vietnam veterans 
(and subsets of them described by 
their potential exposure to Agent 
Orange) are not at increased risk for 
fathering babies with the aggregate 
of all the types of birth defects stud- 
ied here, we found some sutistically 
significant results; however, they may 
not be biologically significant In con- 
sidering these findings, it must be 
kept in mind that many hypotheses 
were tested in this study, and some 
statistically significant differences 
were to be expected, even if no true 
differences in risk exist in the popula- 
tions from which the parents in case 
and control groups were drawn. A 
statistically significant result does 
not necessarily mean that there are 
true differences in risk. One can only 
say, on the basis of the associated 
probability level, a particular finding 
would arise only infrequently because 
of chance vagaries of the sampling 
process. In this circumstance, it 
' seems appropriate to discuss these 
findings in the context of the several 
factors that need to be considered in 
the inferential process. Alternatively, 
it must be kept in mind that this 
study had only a low [>ower to detect 
modestly increased risks for individu- 
al types of defects that have affected 
small numbers of babies. 

An association between spina bifi- 
da and the two Agent Orange EOIs is 
noted— there seem to be increasing 
risks with increasing scores on the 
indices. While there are some differ- 
ences in the epidemiology and em- 
bryology of anencephalus and spina 
bifida, they are generally thought to 
be etiologically related defects." Al- 
though the logistic regression coeffi- 
cients for the indices for anencepha- 
lus are not significant, the point 
estimates are negative, suggesting a 
lower risk for those men who had the 
higher index scores. Therefore, the 
lack of an association between the 
indices and anencephalus suggests 
that the associations with spina bifi- 
da may be chance phenomena. 

Vietnam veterans' risk for fa- 

•■AMA. Aug 17. 1984— Vol 252. No. 7 



thering babies with congenital neo- 
plasms was 1.8 (Table 4), with 95% 
confidence limits of 0.99 to 3.29. The 
regression coefficient associated with 
the Agent Orange EOI based on inter- 
views was significantly greater than 
0.0. The point estimates of the risks 
found here are rather low, of such a 
level that they could conceivably be 
the result of some unknown bias or 
unmeasured confounding factor. They 
could be chance events, or they could 
be the result of some experience in 
the Vietnam service of fathers. The 
same may be said for the positive 
associations noted for cleft lip with or 
without cleft palate (Table 4). 

Vietnam veterans (in general) do 
not seem to have had a greater than 
normal risk of fathering more than 
one baby with birth defects. However, 
a significantly higher proportion of 
men who believed that they had been 
exposed to Agent Orange had a sec- 
ond affected baby (born after the 
affected index baby) than did other 
fathers of babies in the case group 
who believed that they had not been 
exposed or who were not Vietnam 
veterans. Because the control group 
was expected and found to have fewer 
families with affected babies born 
after the index baby than there were 
among the families in the case group, 
they were not used as a point of 
reference. Instead, the comparisons 
were done with families in the case 
e^oup in which the fathers were not 
Vietnam veterans or were Vietnam 
veterans who said that they were not 
exposed to Agent Orange. This ap- 
proach is similar to the approach 
taken for the other analyses of the 
self-reports of Agent Orange expo- 
sure, an approach that was taken for 
the purpose of reducing possible case- 
control bias. (Conceivably, this asso- 
ciation is an expression of a case- 
control bias in which fathers with 
only one affected baby were less like- 
ly to report self-perceived exposure. 

The apparent association between 
malaria and hypospadias is of inter- 
est Malaria infection was a major 
disease problem for military medicine 
in Vietnam." Vietnam veterans' re- 
ports of malaria were not validated, 
as for example by review of medical 
records, but their statements about 
treatment received lend credence to 
their reporU of malaria. 

How do the results of this study 



compare with the results of related 
studies? The most directly compara- 
ble is the study of birth defects risks 
among Australian Vietnam veterans, 
conducted by the Commonwealth In- 
stitute of Health.' It showed, in a 
matched-pair design of 8.517 cases 
and controls, no increased risk of 
all types of structural birth defects 
combined among men who served in 
Vietnam in the Australian Array. 
Kunstadter" reviewed Vietnamese 
hospital records from 1962 through 
1973 and found no increased frequen- 
cies of defects in babies born to 
mothers possibly exposed to herbi- 
cides; his study was not designed to 
show the possible effects of exposure 
of fathers. Tung et al" reported his- 
tories of the families of North Viet- 
namese veterans who had served in 
sprayed areas of the South. He pre- 
sented several case reports of chil- 
dren with birth defects whose parents 
stated that they were sprayed with 
herbicides. The description provided 
no opportunity for comparison with 
families exposed to herbicide who did 
not have children with birth defects. 

In several other studies, male and 
female exposures outside of Vietnam 
have been evaluated,""" but no ad- 
verse human reproductive effects 
have been conclusively demonstrated 
to be related to exposure to pheonoxy 
herbicides and dioxin. Evidence and 
concern for such ill effects come from 
experiments in which laboratory ani- 
mals are used. These adverse out- 
comes occur after chemicals are 
administered to pregnant females at 
critical times during gestation." Ani- 
mal experiments in which paternal 
exposures have been evaluated have 
had negative results." 

The pattern just described is not 
unusual. The ability of drugs and 
infections to cause reproductive prob- 
lems by maternal-fetal exposures is 
well known (eg, thalidomide and 
rubella). (Conversely, there have been 
no unequivocal demonstrations of 
such effects acting through paternal 
exposures." The risks for fathering 
babies with defect syndromes caused 
by fresh dominant mutations (eg, 
achondroplasia) is known to increase 
with increasing paternal age." This 
association was the basis for forming, 
for this study, a special group of 
babies born with defects thought like- 
ly to be caused by fresh dominant 



Vlatnam Veterans— Erickwn at i 



911 



448 



mutations. It is now known that 
about 25% of babies born with triso- 
my 21 (Down's syndrome) derive their 
extra chromosomes from their fa- 
thers." Whether the paternal-age as- 
sociations with dominant mutations 
or the paternal contributions of extra 
chromosomes in Down's syndrome 
are caused by environmental expo- 
sures is unknown. Indeed, the possi- 
bility of more general paternal con- 
tributions to the occurrence of birth 
defects has not been extensively 
investigated. 

The studies of human populations 
with well-documented exposure to 
herbicides and/or dioxin have been 



small. Such small studies have only a 
weak ability to demonstrate even 
modestly increased risks; therefore, 
the fact that no increased risks have 
been demonstrated may reflect the 
weaknesses of the studies rather than 
a true lack of effect. Although the 
present study was large, the esti- 
mates of Agent Orange exposure that 
had to be used were probably rather 
inaccurate. Therefore, the conclusions 
regarding possible Agent Orange- 
associated risks for Vietnam veterans 
that can be dravim from this study are 
weak. Even so, this study provides 
strong evidence that Vietnam veter- 
ans in general are not at increased 



risk. This suggests that if there is any 
increased risk related to exposure to 
Agent Orange, either the risk must be 
small, must be limited to select 
groups of Vietnam veterans, or the 
increased risk must be limited to 
specific types of defects. 



by tlM C«nUre for DiMmM 
Control. CopiM cm b« obuin«d on raquctt from 
th« author! I r«f arance 8). 

Many indiridoala of MvtrtI orginiutiona 
gava halp dariii( tha eouna of thu projact. 
including tha tuB of tha Array Agant Oranga 
Ta*k Porca, Richard C. Chriatian, CRM. diractor. 
tha itifr of Wastat Inc. Martha Barlin. projact 



Vatarana Adrainiatratioo. 



azpoawl to Agant Oranga. JAMA 1979:2422391. 

Z UVacchio PA. Piahayan HM, Singar W: 
Agtnt Oranga and birth dafacta. N Engl J llti 
1983d08:71»-7a). 

1 Donovan JW: Co— Control Study of C<m- 
gnital AKomali— nd Vittnam Strvtc*. Sydney, 



Univaraity of Sydnay, 1983. 

4. Young KL. Calcagni JA. Thalkan CE, tt at 
TSt Taricdon. EnvtmtmnUal Fait, and Hvr 
man Ritk 9/ Htrincidt Orangt and iUAnoeiaUd 
Dtam. US Air Porca Occupatiooal and Environ- 
mantal Health Laboratory (GEIHL) tachnicaJ 
raport TR-Tg-92. Brooks APB. Taza*. Aaroapaea 
Madical Diviaion. 1978. 

5. Prirdman JM: Doei Agant Oranga cauaa 
birth dafacu? TtnUolon 1984;2»:19S-221. 

8. Edmonda LD. Uyda PM. Jaraaa LM. at aL 
CoBganJtal malformationa survaillancc Two 
ima. Ini J Ej)id»mKil 19ema:247. 



T. World Health Organitation: InUrnatianal 
CUuti/Uation (^ DumutM, 1966 rariaion. based 
on tha reeommendationa of tha Eighth Reriaion 
Coo/erance, 19fiS. Genera, World Health Organi- 
tation. 1967, vol 1. 

g. Eridoon JD, Mulinara J, McCIain PW, at aL 
Vittnam VeUnnu' RitJa for Fathtrtng Babia 
Born unlA BntA D^tct*. Atlanta. Centers for 
Diacaae Control 1984. 

9. Saltier CC. Jablon S: Effects of selection on 



R*f«r*fie«s 



for r 



val studies irith tied death tines. 
, 1981;«8:70S-707. 

11. Vaurans Administrstion: Wv<*' (md Aeoi- 
ihsr A Slndy <rf Attitndtt Tottvd Vittnam Era 
Vtfrant. 96th Cong. 2nd seta (1980). Houae 
Conunittae Print No. 88. 

12. Rtvitv of 



Diomu. Analysis of the Ut«ratur«-V101(93)P- 
823. Veterans Administndoo, 1981. vol 1. 

13. Carter Cft Ouee to Che etiology of neural 
tube malformatiooa. Dtv Utd CKdd Snrol 
1974J6(suppi 32):S-1&. 

14. Neel & Vittnam Shufiec Mtdial Support 
of Ou US Army in Vittnam: 19tS-l»n. Oapt of 
Array, 1973. 

15. Kunstadur P A Stndy of Htrbicidu and 
Birth DtftOt in Oxt RtpnUie of Vittnam: An 
Anatytit ofHatpiUU Rteordt. National Acaderay 
Press, 1982. 

16. Tung TT, Anh TK. Tayen BC, et al: Qinieal 
effects of massive snd continuous utilisatioo of 
defoliants 00 civilians: Preliminary survey. Vitt- 
namtm Stndut 1971;2»'.SS-81. 

17. Thomas HP: 2,4>T use and congenital 
malforraation rates in Hungary. LMeat 1980: 
2214-2U. 

la Smith AH. FUher DO. Pearee N. et at 



Zealand 2,4>T Sprayera. Anh Envirm Htaith 
1982^7:197-200. 

19. Hanify JA. Metcalf P. Nobbe CL. et al: 
Aerial spraying of 2.4.S-T aiid human birth 
malformations: An epidemiologic investigatian. 
Satnet 1981:21234».3S1. 

20. Townaend JC. Bodner KM, VsnPeenen PP, 
et al: Survey of reproductive evenu of wives of 
employees exposed U chlorinated dionna. Am J 
EjMrmiol 1982:1 ll-fiSS-Tl 3. 

21. Suakisd RR. Heruberg VS: Human health 
effacu of 2.4.S-T and iu toxic contaminants. 
JAMA 1984251^372-2380. 

22. Courtnay KD, Moore JA: Teratology stud- 
ies with 2,4.5-T and 24.73-TCDD. ToiieoJ Aypl 
Pharmaeoi 19na)-.396-40S. 

23. Lamb JC. Moore JA. Marka TA: Evaiaa- 
tiam of *.i-DJMS-T. and tJ.T.S-TCDD Toxicity 
m CSTBL/S Mica: Rtfroduction and Ftrtility in 
rrsotsd Mait Mict and Evahtatvyn ofCangtnitai 
Malformationt m Thtir Otfiprino. National Tox- 
icology Program report 80-44. Research Triangle 
Park. NC. National Toxicology Program, 1980. 

24. Pears JH Teratogens and the male. Mtd J 
Amt 1983:2:16-20. 

25. Pearoee LS: Paternal age in achondropla- 
sia and mongoliam. Am J Hum Genet 1967; 
9:167-169. 

26. Hook EB. Regal RK: A search for a 
palemal-aga effect upon caaes of 47,'fZl in 
which tha extra chromoeorae ia of paternal 
origin. Am J Hum Gtntt 1984:36:413-421. 



17. 1984— Vol 252. No. 7 

Pnnna »nd PutWis/ied in rfte Unilod i 



Vietnam Veterans— Erickson et ( 



449 



5-12-94 



■ DEN 



NEWS 



(No. 90) 



A-7 



It also would authorize President Clinton's proposed 
environmental technology initiative, which would pro- 
vide grants to aid the development of innovative 
environmental technologies in fiscal 1994 and 1995. 

One title of the bill includes a provision requiring 
EPA to Uke 1.25 percent of superfiind money and use 
it to develop new and efficient cleanup technologies. 

Information would be made available to help small 
businesses fmd environmental technologies to fit their 
needs under an outreach program the bill would 
establish. 

A voluntary program to verify the effectiveness and 
performance of new environmoital technologies to 
ease their entry into the marketplace would be initiat- 
ed under the bill EPA and the Commerce Department 
also would provide assistance to small technology 
companies. 

The House companion bill, HR 3870, has not been 
scheduled for a floor vote since its clearance by the 
Science, Space, and Technology Committee April 14.0 



EPA DRAFT RISK CHARACTERIZATION CITES 
WIDE RANGE OF EFFECTS AT LOW EXPOSURE 

Diozins and related compounds are potent toxicants 
that produce a wide range of effects at very low levels 
when compared to other environmental contaminants, 
according to the Environmental Protection Agency's 
draft risk characterization document obtained by BNA 
May 11. 

But the draft also documented that existing body 



adverse health effects have been detected. 

The 62-page risk characterizatiott document is the 
final chapter of EPA's nine volume revised health risk 
assessment of diozins and related compounds. A risk 
characterization Is one part of the standardized four- 
part health risk assessment It contains a summary of 
the scientific findings from other parts of a risk 
assessment and will be used by EPA regulatory offi- 
cials to aid their decision-making. 

While "a weight-of-«vidence analysis suggests that 
diozins and related compounds are likely to present a 
cancer hazard to humans," the document indicates 
that non-cancer health effects may pose a health 
threat at low exposure levels. 

EPA did not release the draft risk characterization. 
The agency only issued a three paragraph statement 
that said "it would be inappropriate to draw conclu- 
sions from it [the draft risk characterization] at this 
point" 

Diozins are a class of structurally similar chemi- 
cals that are made as a byproduct of several industri- 
al activities, such as incineration and using chlorine 
bleach in pulp and papermaking. TCDD, 2,3,7,8-te- 
trachloro-p-dibenzodiozin is the most studied of the 
family of chemicals. 

Fred Webber, president of the Chemical Manufac- 
turers Association, May U said "Based on what we've 
been told by the EPA. the reassessment will show that 
the margin of safety is probably narrower than the 
agency would like. It also says that although there is 



no need to be alarmed, there Is a need to act. specifi- 
cally to further reduce diozin exposure." 

The CMA sutement said the industry group had not 
seen the entire reassessment document, but it bad 
contacted various EPA officials responsible for the 
reassessment effort 



Of 

The draft risk characterization discussed numerous 
aspects of the related hazard assessment, exposure 
assessment and dose-response parts of the risk assess- 
ment Among the conclusions contained in the report 
were: 

• There is adequate evidence from studies in human 
populations as well as in laboratory animals and other 
experimental data to support the inference that expo- 
sure to diozins and related chemicals causes a "pleth- 
ora" of effects; 

• Based on all the data reviewed in this reassess- 
ment picture emerges of TCDD and related com- 
pounds as potent tozlcants producing a wide range of 
effects at very low levels when compared to other 
environmental contaminants; and 

• Diozin ezposure from multiple sources may result 
in a number of biochemical and biological effects in 
both humans and other animals, many of which are 
considered adverse or tozlc effects, and some of which 
occur at very low levels of exposure. 

"Dioxin and related compounds presents and excel- 
lent example of a case where background levels in 
general population are likely to have a significance 
for evaluation of the relative impact of Incremental 
exposures aiwociated with a specific source," accord- 
ing to the draft risk characterization. 

The document also noted that the scientific commu- 
nity has Identified and described a common initiating 
mechanism that may account for most if not all the 
observed effects in animals 



EPA Rtetlon 

"This whole document is in interagency peer review 
and we're trying to work closely with other agencies 
in the federal government to make sure we're devel- 
oping the best science poesible," David Gardiner. EPA 
assistant administrator for policy, planning, and eval- 
uaUon. told BNA May 11. 

"We look forward to incorporating the comments of 
those agencies before we release it [the draft risk 
characterization] publicly," Gardiner explained. 

Gardiner is co-chair of an internal agency group 
reviewing EPA policies and regulations in light of the 
scientific findings of the reassessment The recently 
formed Diozin Risk Management Coordinating Coun- 
cil Is co-chaired by Gardiner, and Dr. Lynn Goldman. 
EPA assistant administrator for prevention, pesti- 
cides, and tozic substances. 

Goldman issued a statement May 10 describing the 

"This report Is the most eztenslve effort ever under- 
taken to undentand diozin, but It Is still preliminary, 
still subject to scientific and interagency review, and 
quite likely to see some changes," Goldman said. 



Copyrigm e 19»4 by THE BUREAU OF NATX)NAL AFFAIRS. INC.. WutHnQlon, D.C. 20037 



450 



■DEN' 



5-12-94 



She further sUted that federal agencies are working 
to make sure dioxin levels in the environment contin- 
ue to decline. 



Industry, Environmental Reaction 

Reaction to the release of the draft risk character- 
ization came quickly. 

CMA and the Chlorine Chemistry Council, a business 
unit within CMA, said several steps should be taken to 
further characterize the sources of dioxins, both natu- 
ral and manmade. 

"Developing a clearer understanding in this area 
would ensure that we focus our remedial efforts 
where they will do the most good," Webber explained. 
Hopefully, a clearer picture of what actions compa- 
nies might initiate to further reduce dioxin emissions 
will emerge after the entire reassessment document is 
subject to scientific peer review and public conunents, 
the CMA officiai said. 

Greenpeace's Rick Hind called for immediate ac- 
tion to restrict major industrial uses of chlorine and 
chlorinated chemicals that produce dioxins. Green- 
peace has been lobbying EPA to phase out many uses 
of chlorine. Officials from the group told BNA they did 
not have a copy of the May 2 draft risk 
characterization. 

"The EPA's findings indicate a public health emer- 
gency from dioxin t^t is not going to go away until 
industry's addiction to chlorine is broken," Barbara 
Dudley, Greenpeace executive director said. 

Peter de Fur, senior scientist with the Environmen- 
tal Defense Fund, told BNA May 11 that EPA should 
treat dioxins like lead and create an agency wide 
policy to address the risks. 

"EPA needs to adopt policy on dioxin to identify 
dioxin sources and immediately put increased controls 
on them. They also should identify alternatives to 
current processes where dioxin is formed and re- 
leased," de Fur said. 



An Unexpected Release? 

Although many EPA sources said they did not know 
who leaked a copy of the draft risk characterization, 
several sources told BNA they believed the environ- 
menul agency intentionally released it 



About 10 copies of the document were circulated 
May 3 for interagency review and comments, an EPA 
spokesman told BNA May 11. The document was sent 
to other federal agencies that have a "direct interest" 
in EPA's dioxin policy, officials said. Those agencies 
include, the Agriculture Department, the Department 
of Health and Human Services, and the Food and Drug 
Administration. Those comments are due to EPA May 
19, officials said. 

Until a recent press leak, the draft risk character- 
ization was the only draft chapter of the dioxin reas- 
sessment EPA had not released publicly. 

All EPA risk assessments have four components: 
hazard identification, dose-response, exposure assess- 
ment, and risk characterization. Many federal agen- 
cies modeled their risk assessment guidelines and 
practices on the National Academy of Sciences' 1983 
so-called red book. Risk Assessment in the Federal 
Government Managinf/ The Process. 

New Data Prompted Reassessment 



In April 1991, EPA Uunched the scientific i 
ment of the risks associated with exposure to dioxins 
and structurally related chemicals. 

At that time, results from epidemiology studies of 
VS. chemical workers showed evidence that certain 
dioxins were carcinogenic in humans. Prior to the 
release of the studies, a group of scientists met in 
October 1990, at the Banbury Conference center in 
New York and reached consensus on several scientific 
issues associated with dioxin health effects. 

EPA also has a similar project ongoing to reassess 
the dioxin risks to wildlife. That project is ongoing, 
but is not expected to be released in draft form unUl 
late 1994, officials explained. 

The agency is expected to release publicly the draft 
risk characterization and related documents by late 
June. At' that time, the agency also will release re- 
vised versions of the other eight chapters of the dioxin 



Written comments on the entire draft reassessment 
will be accepted for 90 days and one month later the 
documents and comments will be reviewed by a spe- 
cial panel of Science Advisory Board members, agen- 
cy officials explained. 

Text of the draft risk characterization appears in 
Section E.D 



Copyright e 1994 by THE BUREAU OF NATIONAL AFFAIRS. IHC. WisTungtoo, O.C. 20037 
10CO-297«/S4/SO«t1.aO 



451 



MALE-MEDIATED 
DEVELOPMENTAL TOXICITY 

Andrew F. Olshan 

Depaitmem of Epidemiology, Univeraity of Nonh Carolina. Chapel Hill. North 

Carolina 27599 

Elaine M. Faustman^ 

Department of Environmental Health. Univenity of Washington; Child 
Development and Mental Retardation Center. Seattle. Washington 98195 

KEY WORDS; aninui. human, abnormalilies. germ cells, occupauoiu 



INTRODUCTION 

The etiology of many of the adverse reproductive outcomes among humans 
is not well understood. Most epidemiologic and laboratory research focuses 
on maternal factors. Studies of such adverse developmental outcomes as 
spontaneous abortion, low birthweight, and birth defects have assessed 
maternal dr>jg. smoking, alcohol, infectious, and occupational exposures. The 
potential role of paternal exposures has not been extensively investigated, 
partly because of the prevailing view that male-mediated developmental 
effects are unlikely (7). Thus, the acquisition of epidemiologic data and the 
development of a definitive mechanism for male-mediated effects have been 
hindered. However, recent laboratory and epidemiologic investigations have 
reinforced earlier animal data, which suggested that paternal exposures may 
be important. 

This review describes potential mechanisms, highlights new data from both 
laboratory and epidemiologic studies, and points out limitations of previous 
studies and gaps in knowledge. We review studies that use a variety of 
developmental endpoints. including gene mutation, chromosomal abnormal- 
ities, spontaneous abortion, congenital abnormalities, and cancer. The as yet 
unclear relationship of these endpoints to effects on sperm pnxluction and 

'For reprints, please contact Dr. Fauslman. 

159 

1 63-7525/93/05 10-0 1 59S02.00 



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incnccpbaly, whh painten havisg the hlgbnt rbk.' Other phyiictl nulfonnitlons evident it bbth, behaviounl |lta 

pitenul occupidom dut h>Te been ttMciattd with a tioas, tnd t bi^tier Inddence of cancer. Ptmhtnnot^ i 

increased itt of havinf a IWebota child with a bhth defect senn ceU tine of the progeny ma; alao be aOECted. An esaaf 

include fimtcn, ianiton, fiutstty and togging woiken, oftfae model drag uacd to ihow the riaks of paternal eipoM 

pdnten^ and plywood tniU woiken." An Increased tiik of to progeny it cydophotphamid*. 

idUbir^ pretom deliveiy, or of ddhrery of an io&ac who Chronic km doiea of cydeplmvphanildc giren to the ai 

b BnaU fhr gcstaeioDBl age waa esaoelateU whh paternal zu do not aignificandy affect hit fettilit/ and yet produt 

employmant u titUtt or In the texdle taiduttxief .* Though in draontic adverae eScctt oa bit progeny. These effeca « 

moat mdiea the chemkal expoaurea for each occupational dote related and depend ort die length of ihv txeaiinca 

group were not identiiied. In two ttudlea yrheie nposura Wtfs teUccdng the effects of die drug at different stagta « 

mauuud a tignitlcant UKrease in the rlik of ipontaneoua ipennatogeneais and tpctm macuntion. The range of 4GMt 

aboitJOQWaaibund to womawhoae husbands had ioaeaaed on progeny tpana an incrcaK in eaiiy embiyo lots am 

blood lead or odnc mercury concentiatioas before coo- malfonnationi, growtfi letardanon. and behavioural at 

cejxloa^* nonnalitiea.'*^ Puitbennore> ^ nuviving, appartnd) 

Batimates of how much paternal occupational esponut oonnal, progeny of male* treated widt cydophoapha^ 

lneTe»*c« the risk of an adverae effect on the progeny nty produce Htte» with an increased inddence of embryo deaifai 

from 1-5 to 5 dmea dependfaig on die profeiaion and the and malformation*." Intercadngly, in this animal model the 

defect. CouTeraely, many joba ehher hare no advetse eCfccta efBtcts on progeny may be reversed readily by ttoppai 

or Improve die outcome.*' Desphe this, certain paternal treatment widi die drug." The exact molecular mcnh a nlw n s 

occupatknal exposures, including exposure to ftiel conbna- undedying these efCects remain a mystery. 

tion products, organic solvents, and metab sudi as lead It is thus apparent from epldemioiogical stodies im 

and mercury are consistently atsodated with tignificaniiy patetsal exposure* to tome chemical* resoh in abnoctial 

increased rate* of abnormal outcomea. progeny. There is a need for more extensive epidemiologW 

The possibility dut "hfertyle" exposure* of di* father to srudiet and thorough momtoting by governmental agencies «f 

cigarette smoke, akohol, cocaine, and odier agents diat may cfaemicaU that may be impbcatcd. It ia also apparent An 

have adverse cfEtcta should also be addresaed. Aldiougb no animal modeb ham been developed diat are bodi accurate and 

definite evidence eaists that paternal anwtdng or alcohol sensitive in assessing male mediated adverse cflbcts qb 

consumption Causes birth deflects, paternal smoking hu been progeny. These models have, however, been used mainly ta 

associated widi low biith wd^ and Increased perinatal test mutagen*. Infoimation derfvtd from die tnidies of 

mortality In several studies.'" occupational exposure must im>w lead to research to idenii^ 

Therapeudc dmg erpoaures are more readily documented, >hc site(s) of acdon of diese agents. Meanwhile, men occt^ia- 

and diere is information on actual doses. Sevenl studies have tionilly exposed to certain chonicals should b« made aware of 

examined die consequences of treatment of the fidier wldi their increased tiska. They should be counselird to avoid 

cytotoxic drugs. Treatment wiAdiese-ls often aasodited widi cercdn chemical expo»ures before dieir panners conceive, 

impaired fertility, cither transient or permanenL Chudren BBRNAUD ROdAZRB 

bdiered by diese men are no more likely to be malformed FnfcMi 

than odier diildren.'"' No definite conchislon can as yet be BARBaRAFHAIS 

drawn on die eff^ts of cytoioodc drxigs becaase d» numbers fnSnm 

of patiena are too low to detect anytl^ less dun a relatively DepmintomanaacelocyaDd-nsapeabe), 

hi^incieasediisk. McOtBUintitiiy, 

The role of paternal occupadonal exposure in childhood ^^j^^ Qfiv* 

cancer has attracted much attentioa One ofdie most studied ^°*^ 
associations is that between exposure to motor vehicle exhaust 
&imes or the products of combustion engines snd childhood 
leukaemia.*^ Another established association ia that of 
Wilms's tumour in the dbildten of vcfaide mechanics, 
autobody repairmen, and welders."** It is noteworthy diat 
the paternal occupations for iriiicfa an increased lisk of 
childhood cancer has been Identified overlap widi those fot 
which there is evidence of an increased hMidcnce of birdi 
defecta. 

The inherent Unntadoni to most epidemiological and 
clinical studies include sn inability to identify die tpedflc 
cbemicab and m coturol for multiiJe exposures and the time 

of exposure. Well controlled animal studies avoid dies* 

difficulties. Overwhelming experimental evidence exists " t^ 

showing that patenul expoeuce to spcdflc environmental or " ^|SJ_ 

dierapeutic agents restilu in a higher incidence of adversely " " •** 4 " ??!! jj^ 7"^ ^ '^'i'tSSZl 

affected progeny. Many environmental chemical* (for MTJUTut ^^ <i_ n mo nmt>i*^ 

example, lead and dlbtomochkaopropane) and drugs (for „J*S^ 

example, cydophotphasaodc) have been shown to do this. 

Drags oe cavlionncntal ctaemicala u viMch die male is 

cipoaad may be ptcsCBt in his seminal ihiid and thus may n ti m«>4. tum sit »*< waa*M ; 

Greedy sftta die ovulated egg, feitiliiation, or embryonic l^S^TaSsSJiP 

dcvdopmcm. Altcmativciy, drugs or other chemicals may » '^^—^■ty" «»**»' 

adverae^ afltetdicfetua by "ftmoiottaliyahesiag male germ n ■a.^cmmcSSEITim 

cdla. TUc adverae effects diat have been obaetved kidudc „ JVr Cr i7 ^~*' - '' '. ? l '' |l ' ! ;^ V ' T , *' , ' , '' . ? ^ 

lo** bafete and after im(iiantaiion (spoatancoua aboniaBs). m, m u. ■- n«>«>i-^i»>»iB»ia»:K ' 




465 



am til* RoytJ CoUefe of ObtiMriciana «nd 
Gynaecalo(i*a th«t iltere should be one tpedaliit for 900 
deiiveriei will be tenable only if the crend tijwirdi nib- 
•pecioliMtion accdeiate*. A siull tefesal base does not 
provide eoougfa eomplicationt co miintain skills.' 

Apan from ttlpuladng a greater rote for midwivee, die 
lepon tnet not to be too preaoiptiv^ it tccogniaaa that 
purdtaten aad providen ma; agree many difiereu models of 
care. The reauli, howevcTi is dut mucfa of the repoR reads like 
a 100 page mbaioQ statement. It also seems to contain some 
internal contradicdooa. For instance, it arguea that women 
should have the option of a planned bomt btith, especially as 
any JDcreised liak Is atnalt (at least in absolute tenns) and eren 
ifaoae who perceive a risk may niaice a trade off in order to 
realise other galnaHoM aa we do wbeo tramporting our 
fiunlUcs by road. Only a pareotaliat could argue against the 
report on this point, but the in£»tinanon chat the report 
suggests should bfbtm this choice was biased, although the 
report argues throughout that oonplea should be given 
unbiased infbtmatlon. The npon states that any expoaitlon 
on the risk of an unexpected emergency at home slKHild be 
bolaiKxd by evidence from quoted snidiet showing hig)Kr 
interrentioQ rates in Ivotpital; tK« problem is ttut these snidies 
are confounded by different patterns of mldwifety care. The 
repoit advocates, however, that, irrespective of virhere the 
chooses to deliver, a woman's intrapartum care ihotsld be die 
responsibility of tlie same midwife. Peifaaps diii jtist shows 
that unbiased informadon. Cor wtilcb the report makes 
repeated pleas, adats ooty in tfaoae few areas whicfa can be 
resohred empirlcaUy. 

The usual slogan about choice appesn b the report, but it 
is not backed up by ttaoughtfiil discuadon. The tepan cornea 
to the «ie sided conchulon that restrictioni are more Gkety to 
be jtBtiiled in response to a "demaikd for intarcntion rather 
dian a request to avoid it.* Thus dte report argues against 
induction of labour purely at a womaa's te<)uest when *^ere 



are no clinical grounds," but 'clinical grounds* are s funai^ 
among other things, of a person's wishes. Some women rosy 
have s value sy«cm wbereby, given dte probabilities of itt 
various outcomes, induction of labour (or even eiectne 
caesarean secdon] en request is endrely appropriau. Tlio« 
who are sincere about women's sutooomy and whose red 
moiivatian is to foster choice rather tlua patticular ctioins 
must avoid uiy faint of double talk. J could not help oodck^ 
dut day centres for fetal aasesamcnt are condemned withom 
even a mendon (^relevant research.) 

The proposed leorganisadon has considerable implicaiiani 
for midwivea, v<^o as Independent practitioners will ije 
dirccdy expoKd to criticism and Utigacioa Some will rtlidi 
the opportunities for personal and profetaioiul devdopmoi, 
while otbtrs may be reluctant to work irregular bouts or 
accept greater reqioniibility. As midwives become more 
autonomous and assertive it will be important that they do not 
abuse their power and become a banier to the InroWeinent of 
odier professionals. Women ahonld be free to coniuk th^r 
general praetidonaia or obatctriciaAS or to avail themseh^es of 
hospital dinia. The report emhasises that no provider gmy 
should monopolise the provision of services. 

MCHAKOULPORO 



bwituK of Ept4«nleloo Bd MMka SotkM Rotuca, 

SdioelofMedJeiK, 

Lcc(UL.U9U( 




IL«Maii«alrM.l*n 

I r«ta«» I. Knkt MfK, BitM M. ni 



'^Clusters'* of anophthalmia in Britain 

Difficult to implicate berumyl on current evidence 



The campaign ted by the press about a possible link between 
the pesticide benomyl and alleged dusteiing of cases of 
aoofdithalmia— babies bom wldi no eyes— iias prompted die 
fovemmenc to commission research.' The government's 
dilemma is whether to pume tiie quesdon of pestiddea 
and duateting or to investigate all the main causes of 
anophthalmia and how they might be prevented. 

^Thatever is dedded, precise case deflnitioo will be of prime 
importance. Anophthalmia is part of a range of defects 
that iodudea microphttialniia. DifTersBtiating between 
anophthalmia and severe microphthalmia and between 
miciophthahnla and normal eye size nuy lequirc eipert 
ewminarion and agreement on tbe limits of normal eye size. 
Isolated eye d^ccn need difttnguishing from those assodated 
with other malfonnaiions as the underlying causes may differ. 
Overall, between 40% and 73% of case* reported to the 
national congenital maUbmudonsuiveillance scheme (CMSS) 
in Ei^land and Wales and to the European congenital 
malfbtnutions tcgistties (BUROCAT) had other malfor- 
mations (B Bocdng and H Dolk, unpubliabed data).* 

Anophthalmia and microphthalmia may remit from fetal 
damage oocuning tip undl mid-pregnancy due tn a range of 
chtomoiomaJ, genetic and enviionmental causes. Of caaea of 
gii«phifaahnia and microphthalmia reported to tlu European 



regiatries, 16% hmd associated chromosomal aboortnalitiea 
and 13% had other symptoms including genetic syndromes.' 
Fewer than 10% of cases notified to the surveillance scheme in 
England and Wales and 16% noofied in Scodand had 
chromoiomal or genetic factors reported (B Botting aixi H 
Dolk, unpublished dau).' Thb is partly due to registration 
under other maljarmadons, Althou^ a genedc aetiology 
is suspected in most cases of anophthahnla or srrere microph- 
tfaalmia, this can be shown only in the minority of cases 
where there la a detaduble chnimoaomal abnonnaUty or a 
famJiT hiatoiy. No genetic markets are yet available. 



toxins, and drugs. In humans, congenital rubella. Influenza, 
varicella, and paivovina B19 infection have b«e^ associated 
with multiple fetal malfonnaiioaa iaduding micropb- 
thafania." Cases of snophtluUmia or microphthalmia have 
also been repotted in assodatioo with antenatal exposure to 
lysergide, etbambutd, dialidomide, and vitamin A."' 

Bxperimemt on animals suggest a posaftde link between 
benomyl and anophthalmia. Some 43% of the offiquing of 
pregnant tats fed more dian 1000 dmea the estimated dose 
of benomyl received by iktm workers spraying pesdddes 
devdoped maUbrmaiiotia inrhidlng mioophthabnia." 
Expedmoual infectioa of pregnant catde with pesdviius 



466 



Tiiui) cause* fetal eye defeeti, 
iochuling «aophlfaalima.>* In Bcitala 100-300 mcKUno of 
fecoptthy tfaou^c to be due to concenital potivltu* In&ctian 
In ctttle ate tepoited etch ytat." 

In Ensltttd aod Watc« about nine new case* of anophthalmia 
and 1 1 of micropbifaalmia are trotted to the congetsital 
malfbnoatioa luivtillanoe icbeme each year vichin the first 
10 dayt of life. Although uodertepocttng undoubtedly 
occun. Che combined prevalence of anophthalmia and 
mkrophdialmia u birth in England and Wale* for 1981-3 and 
1986-90 WM 0"4 and 03/10000 Uve Unh* ictpccdrdy." 
Theie flgure* are nmilar to the prevalence of 0-VlOOOO live 
binfas for 1985-92 reported by die Ndrtfaem regioaal fatal 
ifanotmality tutvey, which ia beted on nodAcadoo* aate- 
nataSy and up to any age poctnaolly (M Rettwict^ penooal 
commuslcadon). 

Tb« pteralence baaed on nodficadon* to the Euiopean 
!gi«lrica la higher, lot 1980-8 
I was repotted in 03/1 0000 births and mioopb- 
thahnia in 1-4/10000 live births.' The discrepancy between 
reglatrica may be partly due to uadeirepocting in Britain, 
differing caie deflnidoos, and OTcresdmation of prevalence in 
centre* vridi a particular Intereat in ocular abaonnalitica. 

Data showing trend* over time are leaa affected by uadct- 
repottlsg. Since 1971, two yean after beoomyi was Ecczised 
in Britain, no increase in the reported prevalence of ai>- 
ophthalmia and micro^ithalmia haa occurred: the reported 
prcralence for En^and and Wales was 0-4, 0-3, and 0-4/1 000 
Uve births in 1971-5, 1976-80, and 1981-5 letpectively.'" 
Over the past 10 years the tue of benomyl has Men, but 
IOC of its metabolite, catbeadazim, whidi alio catisei ma^ 
fotmidoiu in rats," has faiaeased neuty lOOO-fold since 1965 
(M R Thomas, Ministiy of Agriculture, Fishetiet, and Pood, 
personal coomiunication). These data suggest that benomyl 
and catbendazim are unlikely to b« major cause* of an- 
ophthalmia or severe mioophchalmia in htmuns. 

A French populadon baaed study of 78 cases during 
1979-88 found no trends with time or spsce-dme duster*." 
The largest duster itported by die Obt$tvtr comprised nine 
caies bom in north Liocolnshhc over 12 jtti." No details of 
the proportion with anophthalmia or microphthalmia was 
presented.'* "Qustera" identifled retrotpectivdy, without a 
prior hypothesis and widiout predefined geographical, 
temporal, and diagnostic boundaries, require caudous 
stadsdcal tresmienL" Cases within die cluster may not be 
causally telaud: the duster may be due to chance or 
manlpuktion of boundaries. 



Future research should b« detiyired (O benefit those at risk, . 
and souUe* of dutteiing may not adii